TY - JOUR AU - Chałubińska-Fendler, Justyna AU - Nowicka, Zuzanna AU - Dróżdż, Izabela AU - Graczyk, Łukasz AU - Piotrowski, Grzegorz AU - Tomasik, Bartłomiej AU - Spych, Michał AU - Fijuth, Jacek AU - Papis-Ubych, Anna AU - Kędzierawski, Piotr AU - Kozono, David AU - Fendler, Wojciech TI - Radiation-induced circulating microRNAs linked to echocardiography parameters after radiotherapy JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 13 PY - 2023 PG - 11 SN - 2234-943X DO - 10.3389/fonc.2023.1150979 UR - https://m2.mtmt.hu/api/publication/34000311 ID - 34000311 LA - English DB - MTMT ER - TY - JOUR AU - Duan, Yifan AU - Gu, Jing AU - Shu, Yafei AU - Han, Xiaofei AU - Liang, Qiankun TI - Exosomes MicroRNA Derived from Cardiac Fibroblasts Involved in Radioactive Cardiac Fibrosis Injury JF - ZHONGGUO SHENGWU HUAXUE YU FENZI SHENGWU XUEBAO / CHINESE JOURNAL OF BIOCHEMISTRY AND MOLECULAR BIOLOGY J2 - CHINESE J BIOCHEM MO BIO VL - 39 PY - 2023 IS - 1 SP - 108 EP - 120 PG - 13 SN - 1007-7626 UR - https://m2.mtmt.hu/api/publication/34000385 ID - 34000385 AB - In recent years, it has been found that microRNA (miRNA) carried by exosomes play an important role in the development of tissue and organ fibrosis. However, studies on the relationship between radiation-induced cardiac fibrosis (RICF) and exosomes and their miRNA are very limited. The purpose of this study is to analyze the possible role of radiation-induced exosome miRNA in the development of RICF by bioinformatics. Myocardial fibroblasts (CFs) are the main effector cells of RICF. The CFs were irradiated with 2 Gy X-rays, and radiation-induced exosomes (X-exo) and unirradiated exosomes of CFs (Exo) were extracted by overspeed centrifugation. Then, exosomes were observed and identified with its morphology, NTA concentration, and exosome surface marker proteins such as CD9, CD63, and CD81. Subsequently, RNA-seq technology was used to detect the miRNA expression profiles of Exo and X-exo, then the differentially expressed miRNAs were screened and their potential target genes and enrichment analysis were analyzed. The results showed that, compared with the control group (Exo), 9 miRNAs were up-regulated in the X-exo (| log_2 Fold Change |>1, P<0.05), of these, 8 are the ones with | log_2 Fold Change |>2; 19 miRNAs were down-regulated in the X-exo (| log_2 Fold Change |>1, P <0.05), of these, 12 are the ones with | log_2 Fold Change |>2. TargetScan, miRWalk and miRNADB were used to predict the target genes of differentially expressed miRNAs, and GO and KEGG enrichment analysis were performed. GO enrichment results showed that target genes regulated by differentially expressed miRNAs were mainly involved in biological processes such as protein phosphorylation and cell signal transduction. Those differentially expressed miRNAs were enriched in cytoplasm, cell membrane and other cellular components, playing molecular functions such as protein kinase binding and protein binding. KEGG enrichment results showed that target genes with differentially expressed miRNAs were mainly enriched in PI3K-Akt, MAPK, mTOR, ECM-receptor interaction, cAMP, Wnt, TGF-beta and Notch related signaling pathways. Combing with literatures, it is suggested that differentially expressed exosomal miRNA may promote the development of RICF by regulating the target genes and related signaling pathways. Because the activation regulation of signaling pathways such as MAPK, PI3K/AKT, and mTOR are mainly dependent on the phosphorylation of key molecules, but not on the regulation of the transcriptional level. The detailed mechanism of "Exosomes miRNA mediate radiation bystander effects to promote RICF" will be investigated in future studies, and the signaling pathways such as ECM, cAMP, TGF-beta, Wnt, Notch, Ras, and Rap1 should be the focus. LA - Chinese DB - MTMT ER - TY - JOUR AU - Jalink, E.A. AU - Schonk, A.W. AU - Boon, R.A. AU - Juni, R.P. TI - Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction JF - FRONTIERS IN CARDIOVASCULAR MEDICINE J2 - FRONT CARDIOVASC MED VL - 10 PY - 2023 SN - 2297-055X DO - 10.3389/fcvm.2023.1300375 UR - https://m2.mtmt.hu/api/publication/34538236 ID - 34538236 N1 - Export Date: 27 January 2024 Correspondence Address: Juni, R.P.; Department of Physiology, Netherlands; email: r.juni@amsterdamumc.nl Funding text 1: This work was supported by the European Research Council (ERC Consolidator “NICCA” to RB) and Dutch CardioVascular Alliance-Renal connection to microvascular disease and HFpEF (DCVA-RECONNEXT) fellowship grant to RJ. Acknowledgments AB - Heart failure with preserved ejection fraction (HFpEF) is the largest unmet clinical need in cardiovascular medicine. Despite decades of research, the treatment option for HFpEF is still limited, indicating our ongoing incomplete understanding on the underlying molecular mechanisms. Non-coding RNAs, comprising of microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), are non-protein coding RNA transcripts, which are implicated in various cardiovascular diseases. However, their role in the pathogenesis of HFpEF is unknown. Here, we discuss the role of miRNAs, lncRNAs and circRNAs that are involved in the pathophysiology of HFpEF, namely microvascular dysfunction, inflammation, diastolic dysfunction and cardiac fibrosis. We interrogated clinical evidence and dissected the molecular mechanisms of the ncRNAs by looking at the relevant in vivo and in vitro models that mimic the co-morbidities in patients with HFpEF. Finally, we discuss the potential of ncRNAs as biomarkers and potential novel therapeutic targets for future HFpEF treatment. 2024 Jalink, Schonk, Boon and Juni. LA - English DB - MTMT ER - TY - JOUR AU - Li, H. AU - Li, C. AU - Zheng, T. AU - Wang, Y. AU - Wang, J. AU - Fan, X. AU - Zheng, X. AU - Tian, G. AU - Yuan, Z. AU - Chen, T. TI - Cardiac Fibroblast Activation Induced by Oxygen–Glucose Deprivation Depends on the HIF-1α/miR-212-5p/KLF4 Pathway JF - JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH J2 - J CARDIOVASC TRANSL VL - - PY - 2023 SP - 1 EP - 15 PG - 15 SN - 1937-5387 DO - 10.1007/s12265-023-10360-2 UR - https://m2.mtmt.hu/api/publication/34035675 ID - 34035675 N1 - Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, 277 West Yanta Road, Xi’an, 710061, China Department of Organ Transplantation, Shanghai Changzheng Hospital, Navy Medical University, 415 Fengyang Road, Shanghai, 200001, China Export Date: 26 June 2023; Cited By: 0; Correspondence Address: G. Tian; Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 277 West Yanta Road, 710061, China; email: tiangang@xjtu.edu.cn; Z. Yuan; Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 277 West Yanta Road, 710061, China; email: zuyiyuan@mail.xjtu.edu.cn; T. Chen; Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 277 West Yanta Road, 710061, China; email: chentao0331@xjtu.edu.cn; X. Zheng; Department of Organ Transplantation, Shanghai Changzheng Hospital, Navy Medical University, Shanghai, 415 Fengyang Road, 200001, China; email: zhengxueyang@163.com AB - It is widely accepted that miRNAs play an important role in the pathogenesis of myocardial fibrosis. This study aimed to identify a new pathway of miR-212-5p in the activation of human cardiac fibroblasts (HCFs) induced by oxygen–glucose deprivation (OGD). First, we found that KLF4 protein was markedly decreased in OGD-induced HCFs. Then, bioinformatics analysis and verification experiments were used to identify the existence of an interaction of KLF4 with miR-212-5p. Functional experiments indicated that OGD significantly upregulated the expression of hypoxia inducible factor-1 alpha (HIF-1α) in HCFs, which positively regulated miR-212-5p transcription by binding to its promoter. MiR-212-5p inhibited the expression of Krüppel-like factor 4 (KLF4) protein by binding to the 3’ untranslated coding regions (UTRs) of KLF4 mRNA. Inhibition of miR-212-5p effectively inhibited the activation of OGD-induced HCFs by upregulating KLF4 expression and inhibited cardiac fibrosis in vivo and in vitro. Graphical Abstract: [Figure not available: see fulltext.]. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. LA - English DB - MTMT ER - TY - JOUR AU - Li, Hongbing AU - Li, Chenxing AU - Zheng, Tao AU - Wang, Yaning AU - Wang, Jin AU - Fan, Xiaojuan AU - Zheng, Xueyang AU - Tian, Gang AU - Yuan, Zuyi AU - Chen, Tao TI - Cardiac Fibroblast Activation Induced by Oxygen-Glucose Deprivation Depends on the HIF-1α/miR-212-5p/KLF4 Pathway JF - JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH J2 - J CARDIOVASC TRANSL VL - 16 PY - 2023 IS - 4 SP - 778 EP - 792 PG - 15 SN - 1937-5387 DO - 10.1007/s12265-023-10360-2 UR - https://m2.mtmt.hu/api/publication/34328988 ID - 34328988 AB - It is widely accepted that miRNAs play an important role in the pathogenesis of myocardial fibrosis. This study aimed to identify a new pathway of miR-212-5p in the activation of human cardiac fibroblasts (HCFs) induced by oxygen-glucose deprivation (OGD). First, we found that KLF4 protein was markedly decreased in OGD-induced HCFs. Then, bioinformatics analysis and verification experiments were used to identify the existence of an interaction of KLF4 with miR-212-5p. Functional experiments indicated that OGD significantly upregulated the expression of hypoxia inducible factor-1 alpha (HIF-1a) in HCFs, which positively regulated miR-212-5p transcription by binding to its promoter. MiR-212-5p inhibited the expression of Kruppel-like factor 4 (KLF4) protein by binding to the 3' untranslated coding regions (UTRs) of KLF4 mRNA. Inhibition of miR-212-5p effectively inhibited the activation of OGD-induced HCFs by upregulating KLF4 expression and inhibited cardiac fibrosis in vivo and in vitro. LA - English DB - MTMT ER - TY - JOUR AU - Tavakol, Daniel Naveed AU - Nash, Trevor R. AU - Kim, Youngbin AU - He, Siyu AU - Fleischer, Sharon AU - Graney, Pamela L. AU - Brown, Jessie A. AU - Liberman, Martin AU - Tamargo, Manuel AU - Harken, Andrew AU - Ferrando, Adolfo A. AU - Amundson, Sally AU - Garty, Guy AU - Azizi, Elham AU - Leong, Kam W. AU - Brenner, David J. AU - Vunjak-Novakovic, Gordana TI - Modeling and countering the effects of cosmic radiation using bioengineered human tissues JF - BIOMATERIALS J2 - BIOMATERIALS VL - 301 PY - 2023 PG - 16 SN - 0142-9612 DO - 10.1016/j.biomaterials.2023.122267 UR - https://m2.mtmt.hu/api/publication/34249745 ID - 34249745 LA - English DB - MTMT ER - TY - THES AU - Freiwan, Marah TI - Investigation of the antiremodeling effects of losartan, mirabegron and their combination on the development of doxorubicin-induced chronic cardiotoxicity in a rat model PB - Szegedi Tudományegyetem (SZTE) PY - 2022 SP - 57 DO - 10.14232/phd.11246 UR - https://m2.mtmt.hu/api/publication/33094425 ID - 33094425 AB - Despite the effectiveness of doxorubicin (DOXO) as a chemotherapeutic agent, dose-dependent development of chronic cardiotoxicity limits its application. The angiotensin-II receptor blocker losartan is commonly used to treat cardiac remodeling of various etiologies. The beta-3 adrenergic receptor agonist mirabegron was reported to improve chronic heart failure. Here we investigated the effects of losartan, mirabegron and their combination on the development of DOXO-induced chronic cardiotoxicity. Male Wistar rats were divided into five groups: (i) control; (ii) DOXO-only; (iii) losartan-treated DOXO; (iv) mirabegron-treated DOXO; (v) losartan plus mirabegron-treated DOXO groups. The treatments started 5 weeks after DOXO administration. At week 8, echocardiography was performed. At week 9, left ventricles were prepared for histology, qRT-PCR, and Western blot measurements. Losartan improved diastolic but not systolic dysfunction and ameliorated SERCA2a repression in our DOXO-induced cardiotoxicity model. The DOXO-induced overexpression of Il1 and Il6 was markedly decreased by losartan and mirabegron. Mirabegron and the combination treatment improved systolic and diastolic dysfunction and significantly decreased overexpression of Smad2 and Smad3 in our DOXO-induced cardiotoxicity model. Only mirabegron reduced DOXO-induced cardiac fibrosis significantly. Mirabegron and its combination with losartan seem to be promising therapeutic tools against DOXO-induced chronic cardiotoxicity. LA - English DB - MTMT ER - TY - JOUR AU - Freiwan, Marah AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Szűcs, Gergő AU - Dinh, Hoa AU - Losonczi, Réka Hajnalka AU - Siska, Andrea AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Cserni, Gábor AU - Dux, László AU - Csont, Tamás Bálint AU - Sárközy, Márta TI - Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 4 PG - 28 SN - 1661-6596 DO - 10.3390/ijms23042201 UR - https://m2.mtmt.hu/api/publication/32689754 ID - 32689754 N1 - Funding Agency and Grant Number: NKFIHNational Research, Development & Innovation Office (NRDIO) - Hungary [FK129094, GINOP-2.3.2-15-2016-00040]; Stipendium Hungaricum Program; Ministry of Human Capacities [TKP2021-EGA-32]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund; Stipendium Hungaricum Scholarship; New National Excellence Program of the Ministry of Human Capacities [UNKP-21-3-SZTE-97, UNKP-21-3-SZTE-98, UNKP-20-5-SZTE-166]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; [EFOP-3.6.3VEKOP-16-2017-00009] Funding text: This research was funded by the projects NKFIH FK129094 (to M.S., funder: National Research, Development and Innovation Office), GINOP-2.3.2-15-2016-00040 (to L.D., funder: National Research, Development and Innovation Office), Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation), and by the Ministry of Human Capacities TKP2021-EGA-32 (to T.C., Project no. TKP2021-EGA-32 has been implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-EGA funding scheme.) and by Stipendium Hungaricum Program (to M.S. and L.D., funder: Tempus Public Foundation). M.F. and D.H. were supported by the Stipendium Hungaricum Scholarship (funder: Tempus Public Foundation). M.G.K., Z.Z.A.K., and M.S. were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-21-3-SZTE-97 to M.G.K., UNKP-21-3-SZTE-98 to Z.Z.A.K., and UNKP-20-5-SZTE-166 to M.S., funder: Ministry of Human Capacities). M.S. was supported by the Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences. Z.Z.A.K. and M.G.K. were supported by the EFOP-3.6.3VEKOP-16-2017-00009 project (funder: National Research, Development and Innovation Office). The APC was funded by Stipendium Hungaricum Program (funder: Tempus Public Foundation). AB - Despite the effectiveness of doxorubicin (DOXO) as a chemotherapeutic agent, dose-dependent development of chronic cardiotoxicity limits its application. The angiotensin-II receptor blocker losartan is commonly used to treat cardiac remodeling of various etiologies. The beta-3 adrenergic receptor agonist mirabegron was reported to improve chronic heart failure. Here we investigated the effects of losartan, mirabegron and their combination on the development of DOXO-induced chronic cardiotoxicity. Male Wistar rats were divided into five groups: (i) control; (ii) DOXO-only; (iii) losartan-treated DOXO; (iv) mirabegron-treated DOXO; (v) losartan plus mirabegron-treated DOXO groups. The treatments started 5 weeks after DOXO administration. At week 8, echocardiography was performed. At week 9, left ventricles were prepared for histology, qRT-PCR, and Western blot measurements. Losartan improved diastolic but not systolic dysfunction and ameliorated SERCA2a repression in our DOXO-induced cardiotoxicity model. The DOXO-induced overexpression of Il1 and Il6 was markedly decreased by losartan and mirabegron. Mirabegron and the combination treatment improved systolic and diastolic dysfunction and significantly decreased overexpression of Smad2 and Smad3 in our DOXO-induced cardiotoxicity model. Only mirabegron reduced DOXO-induced cardiac fibrosis significantly. Mirabegron and its combination with losartan seem to be promising therapeutic tools against DOXO-induced chronic cardiotoxicity. LA - English DB - MTMT ER - TY - GEN AU - Kozbenko, Tatiana TI - Space Health Effects Informed Through Application of the Adverse Outcome Pathway Framework PY - 2022 PG - 141 UR - https://m2.mtmt.hu/api/publication/33681437 ID - 33681437 LA - English DB - MTMT ER - TY - JOUR AU - Mpweme Bangando, Harlyne AU - Simard, Christophe AU - Aize, Margaux AU - Lebrun, Alexandre AU - Manrique, Alain AU - Guinamard, Romain TI - TRPM4 Participates in Irradiation-Induced Aortic Valve Remodeling in Mice JF - CANCERS J2 - CANCERS VL - 14 PY - 2022 IS - 18 PG - 20 SN - 2072-6694 DO - 10.3390/cancers14184477 UR - https://m2.mtmt.hu/api/publication/33101181 ID - 33101181 N1 - Funding Agency and Grant Number: French Government [ANR-16-RHUS-0003] Funding text: This work was supported by the French Government, managed by the National Research Agency (ANR) under the program "Investissements d'avenir" with the reference ANR-16-RHUS-0003, and was conducted as part of the FHU CARNAVAL project (GSC G4). AB - Thoracic radiotherapy can lead to cardiac remodeling including valvular stenosis due to fibrosis and calcification. The monovalent non-selective cation channel TRPM4 is known to be involved in calcium handling and to participate in fibroblast transition to myofibroblasts, a phenomenon observed during aortic valve stenosis. The goal of this study was to evaluate if TRPM4 is involved in irradiation-induced aortic valve damage. Four-month-old Trpm4+/+ and Trpm4−/− mice received 10 Gy irradiation at the aortic valve. Cardiac parameters were evaluated by echography until 5 months post-irradiation, then hearts were collected for morphological and histological assessments. At the onset of the protocol, Trpm4+/+ and Trpm4−/− mice exhibited similar maximal aortic valve jet velocity and mean pressure gradient. Five months after irradiation, Trpm4+/+ mice exhibited a significant increase in those parameters, compared to the untreated animals while no variation was detected in Trpm4−/− mice. Morphological analysis revealed that irradiated Trpm4+/+ mice exhibited a 53% significant increase in the aortic valve cusp surface while no significant variation was observed in Trpm4−/− animals. Collagen staining revealed aortic valve fibrosis in irradiated Trpm4+/+ mice but not in irradiated Trpm4−/− animals. It indicates that TRPM4 influences irradiation-induced valvular remodeling. LA - English DB - MTMT ER - TY - JOUR AU - Zhang, Dao-ming AU - Deng, Jun-jian AU - Wu, Yao-gui AU - Tang, Tian AU - Xiong, Lin AU - Zheng, Yong-fa AU - Xu, Xi-ming TI - MicroRNA-223-3p Protect Against Radiation-Induced Cardiac Toxicity by Alleviating Myocardial Oxidative Stress and Programmed Cell Death via Targeting the AMPK Pathway JF - FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY J2 - FRONT CELL DEV BIOL VL - 9 PY - 2022 SN - 2296-634X DO - 10.3389/fcell.2021.801661 UR - https://m2.mtmt.hu/api/publication/32606674 ID - 32606674 LA - English DB - MTMT ER - TY - JOUR AU - Chauhan, Vinita AU - Hamada, Nobuyuki AU - Monceau, Virginie AU - Ebrahimian, Teni AU - Adam, Nadine AU - Wilkins, Ruth C. AU - Sebastian, Soji AU - Patel, Zarana S. AU - Huff, Janice L. AU - Simonetto, Cristoforo AU - Iwasaki, Toshiyasu AU - Kaiser, Jan Christian AU - Salomaa, Sisko AU - Moertl, Simone AU - Azimzadeh, Omid TI - Expert consultation is vital for adverse outcome pathway development: a case example of cardiovascular effects of ionizing radiation JF - INTERNATIONAL JOURNAL OF RADIATION BIOLOGY J2 - INT J RADIAT BIOL VL - 97 PY - 2021 IS - 11 SP - 1516 EP - 1525 PG - 9 SN - 0955-3002 DO - 10.1080/09553002.2021.1969466 UR - https://m2.mtmt.hu/api/publication/32173154 ID - 32173154 LA - English DB - MTMT ER - TY - JOUR AU - Du, Yang AU - Ning, Jin-zhuo TI - MiR-182 Promotes Ischemia/Reperfusion-Induced Acute Kidney Injury in Rat by Targeting FoxO3 JF - UROLOGIA INTERNATIONALIS J2 - UROL INT VL - 105 PY - 2021 IS - 7-8 SP - 687 EP - 696 PG - 10 SN - 0042-1138 DO - 10.1159/000515649 UR - https://m2.mtmt.hu/api/publication/32381577 ID - 32381577 AB - Background: Renal ischemia/reperfusion (I/R) injury (RIRI) is the main cause of acute kidney injury (AKI) in patients. We investigated the role of miR-182 after renal ischemia/reperfusion (I/R) in rat to characterize the microRNA (miRNA) network activated during development and recovery from RIRI. Methods and Results: 12 h after lethal (45 min) renal ischemia, AKI was verified by renal histology (tubular necrosis and regeneration), blood urea nitrogen level, and renal mRNA expression in Wistar rats. We found that miR-182 markedly increased after renal I/R. In cell hypoxia/reoxygenation model, we found similar upregulation of miR-182. In function gain/loss assay, we confirmed an impaired effect of miR-182 and identified Forkhead box O3 (FoxO3) as a direct downstream target of it. By using miR-182 antagomir, the I/R injury was markedly ameliorated. Conclusions: Our results demonstrate that miR-182 promotes cell apoptosis and I/R injury through directly binding to FoxO3. The present study will provide potential therapeutic targets for renal I/R-induced AKI, and open a new avenue for AKI treatment by manipulating miRNAs levels. LA - English DB - MTMT ER - TY - JOUR AU - Fahada, Helmy AU - Suprabawati, Desak Agung AU - Erawati, Dyah TI - The Effect of External Radiotherapy to the Left Ventricle Systolic Function in Locally Advanced Breast Cancer Patients JF - INTERNATIONAL JOURNAL OF RESEARCH AND REVIEW J2 - IJRR VL - 8 PY - 2021 IS - 11 SP - 350 EP - 356 PG - 7 SN - 2454-2237 DO - 10.52403/ijrr.20211143 UR - https://m2.mtmt.hu/api/publication/32532243 ID - 32532243 LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Varga, Zoltán AU - Szűcs, Gergő AU - Freiwan, Marah AU - Farkas, Katalin AU - Kővári, Bence AU - Cserni, Gábor AU - Kriston, András AU - Kovács, Ferenc AU - Horváth, Péter AU - Földesi, Imre AU - Csont, Tamás Bálint AU - Kahán, Zsuzsanna AU - Sárközy, Márta TI - Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 22 PY - 2021 IS - 23 PG - 24 SN - 1661-6596 DO - 10.3390/ijms222312963 UR - https://m2.mtmt.hu/api/publication/32517976 ID - 32517976 N1 - MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Oncotherapy, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, H-6720, Hungary Synthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Szeged, H-6726, Hungary Single-Cell Technologies Ltd, Szeged, H-6726, Hungary Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, 00014, Finland Cited By :1 Export Date: 11 July 2022 Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu LA - English DB - MTMT ER - TY - THES AU - Kovács, Zsuzsanna TI - Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy [A losartan és mirabegron kezelés hatásának összehasonlítása urémiás kardiomiopátia patkány modelljében] PB - Szegedi Tudományegyetem (SZTE) PY - 2021 SP - 48 DO - 10.14232/phd.11064 UR - https://m2.mtmt.hu/api/publication/32868192 ID - 32868192 LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Zsuzsanna AU - Szűcs, Gergő AU - Freiwan, Marah AU - Kovács, Mónika Gabriella AU - Márványkövi, Fanni AU - Dinh, Hoa AU - Siska, Andrea AU - Farkas, Katalin AU - Kovács, Ferenc AU - Kriston, András AU - Horváth, Péter AU - Kővári, Bence AU - Cserni, Bálint Gábor AU - Cserni, Gábor AU - Földesi, Imre AU - Csont, Tamás Bálint AU - Sárközy, Márta TI - Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 11 PY - 2021 IS - 1 PG - 18 SN - 2045-2322 DO - 10.1038/s41598-021-96815-5 UR - https://m2.mtmt.hu/api/publication/32172362 ID - 32172362 N1 - Funding Agency and Grant Number: NKFIHNational Research, Development & Innovation Office (NRDIO) - Hungary [FK129094, K115990, EFOP-3.6.2-16-2017-00006]; Ministry of Human Capacities [20391-3/2018/FEKUSTRAT]; New National Excellence Program of the Ministry of Human Capacities [UNKP-20-5-SZTE-166, UNKP-19-4SZTE-89, UNKP-19-3-SZTE-160, UNKP-19-3-SZTE-159, UNKP-19-2-SZTE-77]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; Szeged Scientists Academy Program; Ministry of Human Resources [TSZ:34232-3/2016/INTFIN]; [GINOP-2.3.2-15-2016 00040]; [EFOP-3.6.3-VEKOP-16-2017-00009] Funding text: The work and publication were supported by the projects GINOP-2.3.2-15-2016 00040, by the NKFIH FK129094 (to M.S.), NKFIH K115990 (to T.C), EFOP-3.6.2-16-2017-00006 (LIVE LONGER), and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). M.S., Z.Z.A.K., M.G.K., and F.M.M., were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-20-5-SZTE-166, UNKP-19-4SZTE-89, UNKP-19-3-SZTE-160, UNKP-19-3-SZTE-159, and UNKP-19-2-SZTE-77). M.S. is supported by the Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences. Z.Z.A.K. and M.G.K. were supported by the EFOP-3.6.3-VEKOP-16-2017-00009 project. FM was supported by the Szeged Scientists Academy Program. The Szeged Scientists Academy Program of the Foundation for the Future of Biomedical Sciences in Szeged is implemented with the support of the Ministry of Human Resources (TSZ:34232-3/2016/INTFIN). LA - English DB - MTMT ER - TY - JOUR AU - Li, L. AU - Nie, X. AU - Zhang, P. AU - Huang, Y. AU - Ma, L. AU - Li, F. AU - Yi, M. AU - Qin, W. AU - Yuan, X. TI - Dexrazoxane ameliorates radiation-induced heart disease in a rat model JF - AGING-US J2 - AGING-US VL - 13 PY - 2021 IS - 3 SP - 3699 EP - 3711 PG - 13 SN - 1945-4589 DO - 10.18632/aging.202332 UR - https://m2.mtmt.hu/api/publication/32016707 ID - 32016707 N1 - Export Date: 15 May 2021 Correspondence Address: Yuan, X.; Department of Oncology, China; email: yuanxianglin@hust.edu.cn AB - Treatment of thoracic tumors with radiotherapy can lead to severe cardiac injury. We investigated the effects of dexrazoxane, a USFDA-approved cardioprotective drug administered with chemotherapy, on radiation-induced heart disease (RIHD) in a rat model. Male Sprague-Dawley rats were irradiated with a single dose of 20 Gy to the heart and treated with dexrazoxane at the time of irradiation and for 12 subsequent weeks. Dexrazoxane suppressed radiation-induced myocardial apoptosis and significantly reversed changes in serum cardiac troponin I levels and histopathological characteristics six months post-radiation. Treatment with dexrazoxane did not alter the radiosensitivity of thoracic tumors in a tumor formation experiment using male nude Balb/C mice with tumors generated by H292 cells. Dexrazoxane reduced the accumulation of reactive oxygen species in rat cardiac tissues, but not in tumors in nude mice. Transcriptome sequencing showed that IKBKE, MAP3K8, NFKBIA, and TLR5, which are involved in Toll-like receptor signaling, may be associated with the anti-RIHD effects of dexrazoxane. Immunohistochemistry revealed that dexrazoxane significantly decreased NF-κB p65 expression in cardiomyocytes. These findings suggest dexrazoxane may protect against RIHD by suppressing apoptosis and oxidative stress in cardiomyocytes. Copyright: © 2020 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. LA - English DB - MTMT ER - TY - JOUR AU - Sárközy, Márta AU - Varga, Zoltán AU - Molnár-Gáspár, Renáta AU - Szűcs, Gergő AU - Kovács, Mónika Gabriella AU - Kovács, Zsuzsanna AU - Dux, László AU - Kahán, Zsuzsanna AU - Csont, Tamás Bálint TI - Pathomechanisms and therapeutic opportunities in radiation‑induced heart disease: from bench to bedside JF - CLINICAL RESEARCH IN CARDIOLOGY J2 - CLIN RES CARDIOL VL - 110 PY - 2021 IS - 4 SP - 507 EP - 531 PG - 25 SN - 1861-0684 DO - 10.1007/s00392-021-01809-y UR - https://m2.mtmt.hu/api/publication/31877554 ID - 31877554 N1 - MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, University of Szeged, Szeged, 6720, Hungary Department of Oncotherapy, Faculty of Medicine, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Export Date: 28 May 2021 Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Kahán, Z.; Department of Oncotherapy, Hungary; email: kahan.zsuzsanna@med.u-szeged.hu Chemicals/CAS: alpha tocopherol, 1406-18-4, 1406-70-8, 52225-20-4, 58-95-7, 59-02-9; amifostine, 20537-88-6; atorvastatin, 134523-00-5, 134523-03-8; captopril, 62571-86-2; colchicine, 64-86-8; enalapril, 75847-73-3; fibroblast growth factor, 62031-54-3; fosinopril, 88889-14-9, 98048-97-6; gelatinase A, 146480-35-5; ibuprofen, 15687-27-1, 79261-49-7, 31121-93-4, 527688-20-6; intercellular adhesion molecule 1, 126547-89-5; interleukin 13, 148157-34-0; interleukin 8, 114308-91-7; interstitial collagenase, 9001-12-1; mevinolin, 75330-75-5; protein kinase B, 148640-14-6; Smad2 protein, 253862-89-4; Smad3 protein, 237417-78-6, 237417-96-8, 237418-00-7; trimetazidine, 13171-25-0, 5011-34-7 Funding details: Hungarian Scientific Research Fund, OTKA Funding details: Magyar Tudományos Akadémia, MTA, EFOP 3.6.3-VEKOP-16-2017-00009 Funding details: Emberi Eroforrások Minisztériuma, EMMI, 20391-3/2018/FEKUSTRAT, UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160, UNKP-19-4-I-SZTE-89, ÚNKP-20-4-SZTE-150, ÚNKP-20-5-SZTE-166 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH; hu:NKFI, EFOP-3.6.2-16-2017-00006, FK129094 Funding details: Wigner Fizikai Kutatóközpont, Magyar Tudományos Akadémia Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open Access funding provided by University of Szeged. The work and publication were supported by the projects GINOP-2.3.2-15-2016-00040, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER) and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, RG, MGK, and ZZAK were supported by the New National Excellence Program of the Ministry of Human Capacities (ÚNKP-20-5-SZTE-166, ÚNKP-20-4-SZTE-150, UNKP-19-4-I-SZTE-89, and UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160). MS is supported by the János Bolyai Research Fellowship of the Hungarian Academy of Sciences. MGK and ZZAK were supported by the EFOP 3.6.3-VEKOP-16-2017-00009. MEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, University of Szeged, Szeged, 6720, Hungary Department of Oncotherapy, Faculty of Medicine, University of Szeged, Szeged, 6720, Hungary Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, H-6720, Hungary Export Date: 29 May 2021 Correspondence Address: Sárközy, M.; MEDICS Research Group, Hungary; email: sarkozy.marta@med.u-szeged.hu Correspondence Address: Csont, T.; MEDICS Research Group, Hungary; email: csont.tamas@med.u-szeged.hu Correspondence Address: Kahán, Z.; Department of Oncotherapy, Hungary; email: kahan.zsuzsanna@med.u-szeged.hu Chemicals/CAS: alpha tocopherol, 1406-18-4, 1406-70-8, 52225-20-4, 58-95-7, 59-02-9; amifostine, 20537-88-6; atorvastatin, 134523-00-5, 134523-03-8; captopril, 62571-86-2; colchicine, 64-86-8; enalapril, 75847-73-3; fibroblast growth factor, 62031-54-3; fosinopril, 88889-14-9, 98048-97-6; gelatinase A, 146480-35-5; ibuprofen, 15687-27-1, 79261-49-7, 31121-93-4, 527688-20-6; intercellular adhesion molecule 1, 126547-89-5; interleukin 13, 148157-34-0; interleukin 8, 114308-91-7; interstitial collagenase, 9001-12-1; mevinolin, 75330-75-5; protein kinase B, 148640-14-6; Smad2 protein, 253862-89-4; Smad3 protein, 237417-78-6, 237417-96-8, 237418-00-7; trimetazidine, 13171-25-0, 5011-34-7 Funding details: Hungarian Scientific Research Fund, OTKA Funding details: Magyar Tudományos Akadémia, MTA, EFOP 3.6.3-VEKOP-16-2017-00009 Funding details: Emberi Eroforrások Minisztériuma, EMMI, 20391-3/2018/FEKUSTRAT, UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160, UNKP-19-4-I-SZTE-89, ÚNKP-20-4-SZTE-150, ÚNKP-20-5-SZTE-166 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH; hu:NKFI, EFOP-3.6.2-16-2017-00006, FK129094 Funding details: Wigner Fizikai Kutatóközpont, Magyar Tudományos Akadémia Funding details: Szegedi Tudományegyetem, SZTE Funding text 1: Open Access funding provided by University of Szeged. The work and publication were supported by the projects GINOP-2.3.2-15-2016-00040, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER) and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, RG, MGK, and ZZAK were supported by the New National Excellence Program of the Ministry of Human Capacities (ÚNKP-20-5-SZTE-166, ÚNKP-20-4-SZTE-150, UNKP-19-4-I-SZTE-89, and UNKP-19-3-SZTE-159, UNKP-19-3-SZTE-160). MS is supported by the János Bolyai Research Fellowship of the Hungarian Academy of Sciences. MGK and ZZAK were supported by the EFOP 3.6.3-VEKOP-16-2017-00009. LA - English DB - MTMT ER - TY - JOUR AU - Peng, Bohui AU - Peng, Chang AU - Luo, Xiaomei AU - Wu, Shuqi AU - Mao, Qian AU - Zhang, Huanting AU - Han, Xiao AU - Wang, Meijing TI - JNK signaling-dependent regulation of histone acetylation are involved in anacardic acid alleviates cardiomyocyte hypertrophy induced by phenylephrine JF - PLOS ONE J2 - PLOS ONE VL - 16 PY - 2021 IS - 12 SP - e0261388 SN - 1932-6203 DO - 10.1371/journal.pone.0261388 UR - https://m2.mtmt.hu/api/publication/32557473 ID - 32557473 LA - English DB - MTMT ER - TY - JOUR AU - Sárközy, Márta AU - Márványkövi, Fanni AU - Szűcs, Gergő AU - Kovács, Zsuzsanna AU - Szabó, Márton Richárd AU - Molnár-Gáspár, Renáta AU - Siska, Andrea AU - Kővári, Bence AU - Cserni, Gábor AU - Földesi, Imre AU - Csont, Tamás Bálint TI - Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females JF - BIOLOGY OF SEX DIFFERENCES J2 - BIOL SEX DIFFER VL - 12 PY - 2021 IS - 1 PG - 20 SN - 2042-6410 DO - 10.1186/s13293-021-00392-1 UR - https://m2.mtmt.hu/api/publication/32191180 ID - 32191180 N1 - Funding Agency and Grant Number: Ministry of Human Capacities [20391-3/2018/FEKUSTRAT, TSZ:34232-3/2016/INTFIN]; New National Excellence Program of the Ministry of Human Capacities [UNKP-20-5-SZTE-166, UNKP-19-4-SZTE-89, UNKP-19-2-SZTE-77, UNKP-20-4-SZTE-150, UNKP19-3-SZTE-269]; Janos Bolyai Research Fellowship of the Hungarian Academy of SciencesHungarian Academy of Sciences; Szeged Scientists Academy Program; [GINOP-2.3.2-152016-00040]; [NKFIH K115990]; [NKFIH FK129094]; [EFOP-3.6.2-16-2017-00006] Funding text: The work and publication were supported by the projects GINOP-2.3.2-152016-00040, NKFIH K115990, NKFIH FK129094, EFOP-3.6.2-16-2017-00006 (LIVE LONGER), and by the Ministry of Human Capacities (20391-3/2018/FEKUSTRAT). MS, FMM, RG, and MRS were supported by the New National Excellence Program of the Ministry of Human Capacities (UNKP-20-5-SZTE-166, UNKP-19-4-SZTE-89, UNKP-19-2-SZTE-77, UNKP-20-4-SZTE-150 and UNKP19-3-SZTE-269). MS is supported by the Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences. FMM was supported by the Szeged Scientists Academy Program. The Szeged Scientists Academy Program of the Foundation for the Future of Biomedical Sciences in Szeged is implemented with the support of the Ministry of Human Capacities (TSZ:34232-3/2016/INTFIN). LA - English DB - MTMT ER - TY - JOUR AU - Tang, N. AU - Dou, X. AU - You, X. AU - Li, Y. AU - Li, X. AU - Liu, G. TI - Androgen Receptors Act as a Tumor Suppressor Gene to Suppress Hepatocellular Carcinoma Cells Progression via miR-122-5p/RABL6 Signaling JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 11 PY - 2021 SN - 2234-943X DO - 10.3389/fonc.2021.756779 UR - https://m2.mtmt.hu/api/publication/32669647 ID - 32669647 N1 - Export Date: 13 February 2022 LA - English DB - MTMT ER - TY - JOUR AU - Bergom, Carmen AU - Rubenstein, Jason AU - Wilson, J. Frank AU - Welsh, Aimee AU - Ibrahim, El-Sayed H. AU - Prior, Phillip AU - Schottstaedt, Aronne M. AU - Eastwood, Daniel AU - Zhang, Mei-Jie AU - Currey, Adam AU - Puckett, Lindsay AU - Strande, Jennifer L. AU - Bradley, Julie A. AU - White, Julia TI - A Pilot Study of Cardiac MRI in Breast Cancer Survivors After Cardiotoxic Chemotherapy and Three-Dimensional Conformal Radiotherapy JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 10 PY - 2020 SN - 2234-943X DO - 10.3389/fonc.2020.506739 UR - https://m2.mtmt.hu/api/publication/31639900 ID - 31639900 LA - English DB - MTMT ER - TY - JOUR AU - Lee, Moon-Sing AU - Liu, Dai-Wei AU - Hung, Shih-Kai AU - Yu, Chih-Chia AU - Chi, Chen-Lin AU - Chiou, Wen-Yen AU - Chen, Liang-Cheng AU - Lin, Ru-Inn AU - Huang, Li-Wen AU - Chew, Chia-Hui AU - Hsu, Feng-Chun AU - Chan, Michael W Y AU - Lin, Hon-Yi TI - Emerging Challenges of Radiation-Associated Cardiovascular Dysfunction (RACVD) in Modern Radiation Oncology: Clinical Practice, Bench Investigation, and Multidisciplinary Care JF - FRONTIERS IN CARDIOVASCULAR MEDICINE J2 - FRONT CARDIOVASC MED VL - 7 PY - 2020 SP - 16 EP - 16 PG - 1 SN - 2297-055X DO - 10.3389/fcvm.2020.00016 UR - https://m2.mtmt.hu/api/publication/31382696 ID - 31382696 AB - Radiotherapy (RT) is a crucial treatment modality in managing cancer patients. However, irradiation dose sprinkling to tumor-adjacent normal tissues is unavoidable, generating treatment toxicities, such as radiation-associated cardiovascular dysfunction (RACVD), particularly for those patients with combined therapies or pre-existing adverse features/comorbidities. Radiation oncologists implement several efforts to decrease heart dose for reducing the risk of RACVD. Even applying the deep-inspiration breath-hold (DIBH) technique, the risk of RACVD is though reduced but still substantial. Besides, available clinical methods are limited for early detecting and managing RACVD. The present study reviewed emerging challenges of RACVD in modern radiation oncology, in terms of clinical practice, bench investigation, and multidisciplinary care. Several molecules are potential for serving as biomarkers and therapeutic targets. Of these, miRNAs, endogenous small non-coding RNAs that function in regulating gene expression, are of particular interest because low-dose irradiation, i.e., 200 mGy (one-tenth of conventional RT daily dose) induces early changes of pro-RACVD miRNA expression. Moreover, several miRNAs, e.g., miR-15b and miR21, involve in the development of RACVD, further demonstrating the potential bio-application in RACVD. Remarkably, many RACVDs are late RT sequelae, characterizing highly irreversible and progressively worse. Thus, multidisciplinary care from oncologists and cardiologists is crucial. Combined managements with commodities control (such as hypertension, hypercholesterolemia, and diabetes), smoking cessation, and close monitoring are recommended. Some agents show abilities for preventing and managing RACVD, such as statins and angiotensin-converting enzyme inhibitors (ACEIs); however, their real roles should be confirmed by further prospective trials. LA - English DB - MTMT ER - TY - JOUR AU - Liu, Jia AU - Kong, Yihui TI - The role of microRNA in myocardial remodeling and heart failure. 微小RNA在心肌重构及心力衰竭中的作用 TS - 微小RNA在心肌重构及心力衰竭中的作用 JF - ZHONGGUO XUN ZHENG YI XUE ZA ZHI / CHINESE JOURNAL OF EVIDENCE-BASED MEDICINE J2 - ZHONGGUO XUN ZHENG YI XUE ZA ZHI VL - 12 PY - 2020 IS - 6 SP - 760 EP - 762 PG - 3 SN - 1672-2531 DO - 10.3969/j.issn.1674-4055.2020.06.30 UR - https://m2.mtmt.hu/api/publication/33681442 ID - 33681442 LA - Chinese DB - MTMT ER - TY - GEN AU - Peng, Bohui AU - Peng, Chang AU - Luo, Xiaomei AU - Huang, Lixin AU - Mao, Qian AU - Zhang, Huanting AU - Han, Xiao TI - Anacardic acid protects against phenylephrine-induced mouse cardiac hypertrophy through JNK signaling-dependent regulation of histone acetylation PY - 2020 EP - 40 PG - 38 UR - https://m2.mtmt.hu/api/publication/31178197 ID - 31178197 AB - Cardiac hypertrophy is a complex process induced by the activation of multiple signaling pathways. We previously reported that anacardic acid (AA), a histone acetylase (HAT) inhibitor, attenuates phenylephrine (PE)-induced cardiac hypertrophy by downregulating histone H3 acetylation at lysine 9 (H3K9ac). Unfortunately, the upstream signaling events remained unknown. The mitogen-activated protein kinase (MAPK) pathway is an important regulator of cardiac hypertrophy. In this study, we explored the role of JNK/MAPK signaling in cardiac hypertrophy. A mouse model of cardiomyocyte hypertrophy was successfully established in vitro using PE. This study showed that p-JNK directly interacts with HATs (P300 and P300/CBP-associated factor, PCAF) and alters H3K9ac. In addition, both the JNK inhibitor SP600125 and the HAT inhibitor AA attenuated p-JNK overexpression and H3K9 hyperacetylation by inhibiting P300 and PCAF during PE-induced cardiomyocyte hypertrophy. Moreover, we demonstrated that both SP600125 and AA attenuate the overexpression of cardiac hypertrophy-related genes (MEF2A, ANP, BNP, and β-MHC), preventing cardiomyocyte hypertrophy and dysfunction. These results revealed a novel mechanism through which AA might protect mice from PE-induced cardiac hypertrophy. In particular, AA inhibits the effects of JNK signaling on HAT-mediated histone acetylation, and could therefore be used to prevent and treat hypertrophic cardiomyopathy.AAanacardic acidANPatrial natriuretic peptideBNPbrain natriuretic peptideCoIPCo-immunoprecipitationHAThistone acetyltransferaseHDAChistone deacetylaseH3K9histone H3 lysine 9H3K9acacetylated lysine 9 on histone H3JNKc-Jun N-terminal KinasePCAFP300/CBP-associated factorPEphenylephrine. LA - English DB - MTMT ER - TY - JOUR AU - Szabó, Márton Richárd AU - Molnár-Gáspár, Renáta AU - Pipicz, Márton AU - Zsindely, Nóra AU - Diószegi, Petra AU - Sárközy, Márta AU - Bodai, László AU - Csont, Tamás Bálint TI - Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 21 PY - 2020 IS - 11 PG - 11 SN - 1661-6596 DO - 10.3390/ijms21113744 UR - https://m2.mtmt.hu/api/publication/31330253 ID - 31330253 N1 - Cited By :5 Export Date: 20 June 2022 LA - English DB - MTMT ER - TY - JOUR AU - Wu, J. AU - Zhang, T. AU - Chen, Y. AU - Ha, S. TI - MiR-139-5p influences hepatocellular carcinoma cell invasion and proliferation capacities via decreasing SLITRK4 expression JF - BIOSCIENCE REPORTS J2 - BIOSCIENCE REP VL - 40 PY - 2020 IS - 5 SN - 0144-8463 DO - 10.1042/BSR20193295 UR - https://m2.mtmt.hu/api/publication/31382695 ID - 31382695 N1 - Department of Hepatobiliary Surgery, Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, 010000, China Department of Geriatric Medicine, Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, 010000, China Cited By :1 Export Date: 17 July 2020 CODEN: BRPTD Correspondence Address: Ha, S.; Department of Geriatric Medicine, Affiliated Hospital of Inner Mongolia Medical UniversityChina; email: hasigaowa2019@163.com LA - English DB - MTMT ER -