@article{MTMT:34000311,
	title = {Radiation-induced circulating microRNAs linked to echocardiography parameters after radiotherapy},
	url = {https://m2.mtmt.hu/api/publication/34000311},
	author = {Chałubińska-Fendler, Justyna and Nowicka, Zuzanna and Dróżdż, Izabela and Graczyk, Łukasz and Piotrowski, Grzegorz and Tomasik, Bartłomiej and Spych, Michał and Fijuth, Jacek and Papis-Ubych, Anna and Kędzierawski, Piotr and Kozono, David and Fendler, Wojciech},
	doi = {10.3389/fonc.2023.1150979},
	journal-iso = {FRONT ONCOL},
	journal = {FRONTIERS IN ONCOLOGY},
	volume = {13},
	unique-id = {34000311},
	issn = {2234-943X},
	year = {2023},
	eissn = {2234-943X}
}

@article{MTMT:34000385,
	title = {Exosomes MicroRNA Derived from Cardiac Fibroblasts Involved in Radioactive Cardiac Fibrosis Injury},
	url = {https://m2.mtmt.hu/api/publication/34000385},
	author = {Duan, Yifan and Gu, Jing and Shu, Yafei and Han, Xiaofei and Liang, Qiankun},
	journal-iso = {CHINESE J BIOCHEM MO BIO},
	journal = {ZHONGGUO SHENGWU HUAXUE YU FENZI SHENGWU XUEBAO / CHINESE JOURNAL OF BIOCHEMISTRY AND MOLECULAR BIOLOGY},
	volume = {39},
	unique-id = {34000385},
	issn = {1007-7626},
	abstract = {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.},
	year = {2023},
	pages = {108-120}
}

@article{MTMT:34538236,
	title = {Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction},
	url = {https://m2.mtmt.hu/api/publication/34538236},
	author = {Jalink, E.A. and Schonk, A.W. and Boon, R.A. and Juni, R.P.},
	doi = {10.3389/fcvm.2023.1300375},
	journal-iso = {FRONT CARDIOVASC MED},
	journal = {FRONTIERS IN CARDIOVASCULAR MEDICINE},
	volume = {10},
	unique-id = {34538236},
	issn = {2297-055X},
	abstract = {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.},
	keywords = {Biomarkers; Therapeutic targets; circRNAs; HFpEF; lncRNAs; HFpEF pathophysiology; non-coding RNAs: miRNAs},
	year = {2023},
	eissn = {2297-055X}
}

@article{MTMT:34035675,
	title = {Cardiac Fibroblast Activation Induced by Oxygen–Glucose Deprivation Depends on the HIF-1α/miR-212-5p/KLF4 Pathway},
	url = {https://m2.mtmt.hu/api/publication/34035675},
	author = {Li, H. and Li, C. and Zheng, T. and Wang, Y. and Wang, J. and Fan, X. and Zheng, X. and Tian, G. and Yuan, Z. and Chen, T.},
	doi = {10.1007/s12265-023-10360-2},
	journal-iso = {J CARDIOVASC TRANSL},
	journal = {JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH},
	volume = {-},
	unique-id = {34035675},
	issn = {1937-5387},
	abstract = {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.},
	keywords = {KLF4; myocardial fibrosis; HIF-1α; Cardiac fibroblasts; OGD; miR-212-5p},
	year = {2023},
	eissn = {1937-5395},
	pages = {1-15}
}

@article{MTMT:34328988,
	title = {Cardiac Fibroblast Activation Induced by Oxygen-Glucose Deprivation Depends on the HIF-1α/miR-212-5p/KLF4 Pathway},
	url = {https://m2.mtmt.hu/api/publication/34328988},
	author = {Li, Hongbing and Li, Chenxing and Zheng, Tao and Wang, Yaning and Wang, Jin and Fan, Xiaojuan and Zheng, Xueyang and Tian, Gang and Yuan, Zuyi and Chen, Tao},
	doi = {10.1007/s12265-023-10360-2},
	journal-iso = {J CARDIOVASC TRANSL},
	journal = {JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH},
	volume = {16},
	unique-id = {34328988},
	issn = {1937-5387},
	abstract = {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.},
	keywords = {KLF4; myocardial fibrosis; Cardiac fibroblasts; HIF-1 alpha; OGD; miR-212-5p},
	year = {2023},
	eissn = {1937-5395},
	pages = {778-792}
}

@article{MTMT:34249745,
	title = {Modeling and countering the effects of cosmic radiation using bioengineered human tissues},
	url = {https://m2.mtmt.hu/api/publication/34249745},
	author = {Tavakol, Daniel Naveed and Nash, Trevor R. and Kim, Youngbin and He, Siyu and Fleischer, Sharon and Graney, Pamela L. and Brown, Jessie A. and Liberman, Martin and Tamargo, Manuel and Harken, Andrew and Ferrando, Adolfo A. and Amundson, Sally and Garty, Guy and Azizi, Elham and Leong, Kam W. and Brenner, David J. and Vunjak-Novakovic, Gordana},
	doi = {10.1016/j.biomaterials.2023.122267},
	journal-iso = {BIOMATERIALS},
	journal = {BIOMATERIALS},
	volume = {301},
	unique-id = {34249745},
	issn = {0142-9612},
	keywords = {HEART; RADIATION; bone marrow; Tissue Engineering; Organs on chip; Space health},
	year = {2023},
	eissn = {1878-5905},
	orcid-numbers = {Kim, Youngbin/0000-0003-1919-1575}
}

@mastersthesis{MTMT:33094425,
	title = {Investigation of the antiremodeling effects of losartan, mirabegron and their combination on the development of doxorubicin-induced chronic cardiotoxicity in a rat model},
	url = {https://m2.mtmt.hu/api/publication/33094425},
	author = {Freiwan, Marah},
	doi = {10.14232/phd.11246},
	publisher = {SZTE},
	unique-id = {33094425},
	abstract = {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.},
	year = {2022}
}

@article{MTMT:32689754,
	title = {Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model},
	url = {https://m2.mtmt.hu/api/publication/32689754},
	author = {Freiwan, Marah and Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Szűcs, Gergő and Dinh, Hoa and Losonczi, Réka Hajnalka and Siska, Andrea and Kriston, András and Kovács, Ferenc and Horváth, Péter and Földesi, Imre and Cserni, Gábor and Dux, László and Csont, Tamás Bálint and Sárközy, Márta},
	doi = {10.3390/ijms23042201},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32689754},
	issn = {1661-6596},
	abstract = {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.},
	keywords = {heart failure; diastolic dysfunction; Cardiac fibrosis; angiotensin II receptor blocker; cardiac inflammation; TGF-beta/SMAD signaling pathway; Onco-cardiology; doxorubicin-induced chronic cardiotoxicity; beta-3 adrenoceptor agonist; sarcoendoplasmic reticulum calcium ATPase 2a},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Freiwan, Marah/0000-0002-2482-0367; Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Szűcs, Gergő/0000-0003-1874-2718; Losonczi, Réka Hajnalka/0009-0001-7220-2184; Földesi, Imre/0000-0002-3329-8136; Cserni, Gábor/0000-0003-1344-7744; Dux, László/0000-0002-1270-1678; Csont, Tamás Bálint/0000-0001-5792-2768; Sárközy, Márta/0000-0002-5929-2146}
}

@misc{MTMT:33681437,
	title = {Space Health Effects Informed Through Application of the Adverse Outcome Pathway Framework},
	url = {https://m2.mtmt.hu/api/publication/33681437},
	author = {Kozbenko, Tatiana},
	unique-id = {33681437},
	year = {2022}
}

@article{MTMT:33101181,
	title = {TRPM4 Participates in Irradiation-Induced Aortic Valve Remodeling in Mice},
	url = {https://m2.mtmt.hu/api/publication/33101181},
	author = {Mpweme Bangando, Harlyne and Simard, Christophe and Aize, Margaux and Lebrun, Alexandre and Manrique, Alain and Guinamard, Romain},
	doi = {10.3390/cancers14184477},
	journal-iso = {CANCERS},
	journal = {CANCERS},
	volume = {14},
	unique-id = {33101181},
	abstract = {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.},
	year = {2022},
	eissn = {2072-6694}
}

@article{MTMT:32606674,
	title = {MicroRNA-223-3p Protect Against Radiation-Induced Cardiac Toxicity by Alleviating Myocardial Oxidative Stress and Programmed Cell Death via Targeting the AMPK Pathway},
	url = {https://m2.mtmt.hu/api/publication/32606674},
	author = {Zhang, Dao-ming and Deng, Jun-jian and Wu, Yao-gui and Tang, Tian and Xiong, Lin and Zheng, Yong-fa and Xu, Xi-ming},
	doi = {10.3389/fcell.2021.801661},
	journal-iso = {FRONT CELL DEV BIOL},
	journal = {FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY},
	volume = {9},
	unique-id = {32606674},
	issn = {2296-634X},
	year = {2022},
	eissn = {2296-634X}
}

@article{MTMT:32173154,
	title = {Expert consultation is vital for adverse outcome pathway development: a case example of cardiovascular effects of ionizing radiation},
	url = {https://m2.mtmt.hu/api/publication/32173154},
	author = {Chauhan, Vinita and Hamada, Nobuyuki and Monceau, Virginie and Ebrahimian, Teni and Adam, Nadine and Wilkins, Ruth C. and Sebastian, Soji and Patel, Zarana S. and Huff, Janice L. and Simonetto, Cristoforo and Iwasaki, Toshiyasu and Kaiser, Jan Christian and Salomaa, Sisko and Moertl, Simone and Azimzadeh, Omid},
	doi = {10.1080/09553002.2021.1969466},
	journal-iso = {INT J RADIAT BIOL},
	journal = {INTERNATIONAL JOURNAL OF RADIATION BIOLOGY},
	volume = {97},
	unique-id = {32173154},
	issn = {0955-3002},
	year = {2021},
	eissn = {1362-3095},
	pages = {1516-1525},
	orcid-numbers = {Chauhan, Vinita/0000-0002-4498-0915; Hamada, Nobuyuki/0000-0003-2518-6131; Wilkins, Ruth C./0000-0002-9621-477X; Patel, Zarana S./0000-0003-0996-6381; Simonetto, Cristoforo/0000-0003-4816-3514; Moertl, Simone/0000-0003-0644-0878}
}

@article{MTMT:32381577,
	title = {MiR-182 Promotes Ischemia/Reperfusion-Induced Acute Kidney Injury in Rat by Targeting FoxO3},
	url = {https://m2.mtmt.hu/api/publication/32381577},
	author = {Du, Yang and Ning, Jin-zhuo},
	doi = {10.1159/000515649},
	journal-iso = {UROL INT},
	journal = {UROLOGIA INTERNATIONALIS},
	volume = {105},
	unique-id = {32381577},
	issn = {0042-1138},
	abstract = {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.},
	keywords = {APOPTOSIS; PROLIFERATION; acute kidney injury; ISCHEMIA REPERFUSION INJURY; miR-182; FOXO3},
	year = {2021},
	eissn = {1423-0399},
	pages = {687-696}
}

@article{MTMT:32532243,
	title = {The Effect of External Radiotherapy to the Left Ventricle Systolic Function in Locally Advanced Breast Cancer Patients},
	url = {https://m2.mtmt.hu/api/publication/32532243},
	author = {Fahada, Helmy and Suprabawati, Desak Agung and Erawati, Dyah},
	doi = {10.52403/ijrr.20211143},
	journal-iso = {IJRR},
	journal = {INTERNATIONAL JOURNAL OF RESEARCH AND REVIEW},
	volume = {8},
	unique-id = {32532243},
	issn = {2454-2237},
	year = {2021},
	eissn = {2349-9788},
	pages = {350-356}
}

@article{MTMT:32517976,
	title = {Investigation of the Antihypertrophic and Antifibrotic Effects of Losartan in a Rat Model of Radiation-Induced Heart Disease},
	url = {https://m2.mtmt.hu/api/publication/32517976},
	author = {Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Varga, Zoltán and Szűcs, Gergő and Freiwan, Marah and Farkas, Katalin and Kővári, Bence and Cserni, Gábor and Kriston, András and Kovács, Ferenc and Horváth, Péter and Földesi, Imre and Csont, Tamás Bálint and Kahán, Zsuzsanna and Sárközy, Márta},
	doi = {10.3390/ijms222312963},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {32517976},
	issn = {1661-6596},
	year = {2021},
	eissn = {1422-0067},
	orcid-numbers = {Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Varga, Zoltán/0000-0001-8537-6282; Szűcs, Gergő/0000-0003-1874-2718; Freiwan, Marah/0000-0002-2482-0367; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768; Kahán, Zsuzsanna/0000-0002-5021-8775; Sárközy, Márta/0000-0002-5929-2146}
}

@mastersthesis{MTMT:32868192,
	title = {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]},
	url = {https://m2.mtmt.hu/api/publication/32868192},
	author = {Kovács, Zsuzsanna},
	doi = {10.14232/phd.11064},
	publisher = {SZTE},
	unique-id = {32868192},
	year = {2021},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579}
}

@article{MTMT:32172362,
	title = {Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy},
	url = {https://m2.mtmt.hu/api/publication/32172362},
	author = {Kovács, Zsuzsanna and Szűcs, Gergő and Freiwan, Marah and Kovács, Mónika Gabriella and Márványkövi, Fanni and Dinh, Hoa and Siska, Andrea and Farkas, Katalin and Kovács, Ferenc and Kriston, András and Horváth, Péter and Kővári, Bence and Cserni, Bálint Gábor and Cserni, Gábor and Földesi, Imre and Csont, Tamás Bálint and Sárközy, Márta},
	doi = {10.1038/s41598-021-96815-5},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32172362},
	issn = {2045-2322},
	year = {2021},
	eissn = {2045-2322},
	orcid-numbers = {Kovács, Zsuzsanna/0000-0002-4197-4579; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Mónika Gabriella/0000-0002-5756-4662; Márványkövi, Fanni/0000-0002-5114-1319; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768; Sárközy, Márta/0000-0002-5929-2146}
}

@article{MTMT:32016707,
	title = {Dexrazoxane ameliorates radiation-induced heart disease in a rat model},
	url = {https://m2.mtmt.hu/api/publication/32016707},
	author = {Li, L. and Nie, X. and Zhang, P. and Huang, Y. and Ma, L. and Li, F. and Yi, M. and Qin, W. and Yuan, X.},
	doi = {10.18632/aging.202332},
	journal-iso = {AGING-US},
	journal = {AGING-US},
	volume = {13},
	unique-id = {32016707},
	issn = {1945-4589},
	abstract = {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.},
	keywords = {APOPTOSIS; Reactive oxygen species; RAT MODEL; dexrazoxane; radiation-induced heart disease},
	year = {2021},
	eissn = {1945-4589},
	pages = {3699-3711}
}

@article{MTMT:31877554,
	title = {Pathomechanisms and therapeutic opportunities in radiation‑induced heart disease: from bench to bedside},
	url = {https://m2.mtmt.hu/api/publication/31877554},
	author = {Sárközy, Márta and Varga, Zoltán and Molnár-Gáspár, Renáta and Szűcs, Gergő and Kovács, Mónika Gabriella and Kovács, Zsuzsanna and Dux, László and Kahán, Zsuzsanna and Csont, Tamás Bálint},
	doi = {10.1007/s00392-021-01809-y},
	journal-iso = {CLIN RES CARDIOL},
	journal = {CLINICAL RESEARCH IN CARDIOLOGY},
	volume = {110},
	unique-id = {31877554},
	issn = {1861-0684},
	year = {2021},
	eissn = {1861-0692},
	pages = {507-531},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Varga, Zoltán/0000-0001-8537-6282; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Mónika Gabriella/0000-0002-5756-4662; Kovács, Zsuzsanna/0000-0002-4197-4579; Dux, László/0000-0002-1270-1678; Kahán, Zsuzsanna/0000-0002-5021-8775; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32557473,
	title = {JNK signaling-dependent regulation of histone acetylation are involved in anacardic acid alleviates cardiomyocyte hypertrophy induced by phenylephrine},
	url = {https://m2.mtmt.hu/api/publication/32557473},
	author = {Peng, Bohui and Peng, Chang and Luo, Xiaomei and Wu, Shuqi and Mao, Qian and Zhang, Huanting and Han, Xiao and Wang, Meijing},
	doi = {10.1371/journal.pone.0261388},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {16},
	unique-id = {32557473},
	issn = {1932-6203},
	year = {2021},
	eissn = {1932-6203},
	pages = {e0261388},
	orcid-numbers = {Wu, Shuqi/0000-0001-7355-8337}
}

@article{MTMT:32191180,
	title = {Ischemic preconditioning protects the heart against ischemia-reperfusion injury in chronic kidney disease in both males and females},
	url = {https://m2.mtmt.hu/api/publication/32191180},
	author = {Sárközy, Márta and Márványkövi, Fanni and Szűcs, Gergő and Kovács, Zsuzsanna and Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Siska, Andrea and Kővári, Bence and Cserni, Gábor and Földesi, Imre and Csont, Tamás Bálint},
	doi = {10.1186/s13293-021-00392-1},
	journal-iso = {BIOL SEX DIFFER},
	journal = {BIOLOGY OF SEX DIFFERENCES},
	volume = {12},
	unique-id = {32191180},
	year = {2021},
	eissn = {2042-6410},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Márványkövi, Fanni/0000-0002-5114-1319; Szűcs, Gergő/0000-0003-1874-2718; Kovács, Zsuzsanna/0000-0002-4197-4579; Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Földesi, Imre/0000-0002-3329-8136; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32669647,
	title = {Androgen Receptors Act as a Tumor Suppressor Gene to Suppress Hepatocellular Carcinoma Cells Progression via miR-122-5p/RABL6 Signaling},
	url = {https://m2.mtmt.hu/api/publication/32669647},
	author = {Tang, N. and Dou, X. and You, X. and Li, Y. and Li, X. and Liu, G.},
	doi = {10.3389/fonc.2021.756779},
	journal-iso = {FRONT ONCOL},
	journal = {FRONTIERS IN ONCOLOGY},
	volume = {11},
	unique-id = {32669647},
	issn = {2234-943X},
	year = {2021},
	eissn = {2234-943X}
}

@article{MTMT:31639900,
	title = {A Pilot Study of Cardiac MRI in Breast Cancer Survivors After Cardiotoxic Chemotherapy and Three-Dimensional Conformal Radiotherapy},
	url = {https://m2.mtmt.hu/api/publication/31639900},
	author = {Bergom, Carmen and Rubenstein, Jason and Wilson, J. Frank and Welsh, Aimee and Ibrahim, El-Sayed H. and Prior, Phillip and Schottstaedt, Aronne M. and Eastwood, Daniel and Zhang, Mei-Jie and Currey, Adam and Puckett, Lindsay and Strande, Jennifer L. and Bradley, Julie A. and White, Julia},
	doi = {10.3389/fonc.2020.506739},
	journal-iso = {FRONT ONCOL},
	journal = {FRONTIERS IN ONCOLOGY},
	volume = {10},
	unique-id = {31639900},
	issn = {2234-943X},
	year = {2020},
	eissn = {2234-943X}
}

@article{MTMT:31382696,
	title = {Emerging Challenges of Radiation-Associated Cardiovascular Dysfunction (RACVD) in Modern Radiation Oncology: Clinical Practice, Bench Investigation, and Multidisciplinary Care},
	url = {https://m2.mtmt.hu/api/publication/31382696},
	author = {Lee, Moon-Sing and Liu, Dai-Wei and Hung, Shih-Kai and Yu, Chih-Chia and Chi, Chen-Lin and Chiou, Wen-Yen and Chen, Liang-Cheng and Lin, Ru-Inn and Huang, Li-Wen and Chew, Chia-Hui and Hsu, Feng-Chun and Chan, Michael W Y and Lin, Hon-Yi},
	doi = {10.3389/fcvm.2020.00016},
	journal-iso = {FRONT CARDIOVASC MED},
	journal = {FRONTIERS IN CARDIOVASCULAR MEDICINE},
	volume = {7},
	unique-id = {31382696},
	issn = {2297-055X},
	abstract = {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.},
	keywords = {TOXICITY; RADIATION; miRNA; Cardiovascular dysfunction; late sequelae},
	year = {2020},
	eissn = {2297-055X},
	pages = {16-16}
}

@article{MTMT:33681442,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/33681442},
	author = {Liu, Jia and Kong, Yihui},
	doi = {10.3969/j.issn.1674-4055.2020.06.30},
	journal-iso = {ZHONGGUO XUN ZHENG YI XUE ZA ZHI},
	journal = {ZHONGGUO XUN ZHENG YI XUE ZA ZHI / CHINESE JOURNAL OF EVIDENCE-BASED MEDICINE},
	volume = {12},
	unique-id = {33681442},
	issn = {1672-2531},
	year = {2020},
	pages = {760-762}
}

@misc{MTMT:31178197,
	title = {Anacardic acid protects against phenylephrine-induced mouse cardiac hypertrophy through JNK signaling-dependent regulation of histone acetylation},
	url = {https://m2.mtmt.hu/api/publication/31178197},
	author = {Peng, Bohui and Peng, Chang and Luo, Xiaomei and Huang, Lixin and Mao, Qian and Zhang, Huanting and Han, Xiao},
	unique-id = {31178197},
	abstract = {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.},
	year = {2020},
	pages = {2-40}
}

@article{MTMT:31330253,
	title = {Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts},
	url = {https://m2.mtmt.hu/api/publication/31330253},
	author = {Szabó, Márton Richárd and Molnár-Gáspár, Renáta and Pipicz, Márton and Zsindely, Nóra and Diószegi, Petra and Sárközy, Márta and Bodai, László and Csont, Tamás Bálint},
	doi = {10.3390/ijms21113744},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31330253},
	issn = {1661-6596},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Szabó, Márton Richárd/0000-0003-0415-5192; Molnár-Gáspár, Renáta/0000-0001-9673-4532; Pipicz, Márton/0000-0002-0944-1684; Zsindely, Nóra/0000-0002-6189-3100; Diószegi, Petra/0000-0001-8109-2266; Sárközy, Márta/0000-0002-5929-2146; Bodai, László/0000-0001-8411-626X; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:31382695,
	title = {MiR-139-5p influences hepatocellular carcinoma cell invasion and proliferation capacities via decreasing SLITRK4 expression},
	url = {https://m2.mtmt.hu/api/publication/31382695},
	author = {Wu, J. and Zhang, T. and Chen, Y. and Ha, S.},
	doi = {10.1042/BSR20193295},
	journal-iso = {BIOSCIENCE REP},
	journal = {BIOSCIENCE REPORTS},
	volume = {40},
	unique-id = {31382695},
	issn = {0144-8463},
	keywords = {ARTICLE; signal transduction; TUMOR INVASION; human; protein analysis; gene expression regulation; membrane protein; controlled study; Gene Targeting; human cell; unclassified drug; protein expression; messenger rna; human tissue; cancer growth; RNA binding; microRNA; liver cell carcinoma; liver carcinogenesis; gene function; RNA analysis; 3' untranslated region; molecular pathology; cancer prognosis; Liver tissue; luciferase assay; gene knockdown; microRNA 139 5p; SLIT and NTRK like family member 4},
	year = {2020},
	eissn = {1573-4935}
}