@article{MTMT:34836146,
	title = {The anti-leprosy drug clofazimine reduces polyQ toxicity through activation of PPARγ},
	url = {https://m2.mtmt.hu/api/publication/34836146},
	author = {Li, Xuexin and Hernandez, Ivó and Koyuncu, Seda and Kis, Balázs and Häggblad, Maria and Lidemalm, Louise and Abbas, Anna Anoir and Sramkó, Bendegúz Gábor and Göblös, Anikó and Brautigam, Lars and Lucas, Jose J. and Carreras-Puigvert, Jordi and Hühn, Daniela and Pircs, Karolina Milena and Vilchez, David and Fernandez-Capetillo, Oscar},
	doi = {10.1016/j.ebiom.2024.105124},
	journal-iso = {EBIOMEDICINE},
	journal = {EBIOMEDICINE},
	volume = {103},
	unique-id = {34836146},
	issn = {2352-3964},
	abstract = {Background: PolyQ diseases are autosomal dominant neurodegenerative disorders caused by the expansion of CAG repeats. While of slow progression, these diseases are ultimately fatal and lack effective therapies.
		
		Methods: A high-throughput chemical screen was conducted to identify drugs that lower the toxicity of a protein containing the first exon of Huntington's disease (HD) protein huntingtin (HTT) harbouring 94 glutamines (Htt-Q94). Candidate drugs were tested in a wide range of in vitro and in vivo models of polyQ toxicity.
		
		Findings: The chemical screen identified the anti-leprosy drug clofazimine as a hit, which was subsequently validated in several in vitro models. Computational analyses of transcriptional signatures revealed that the effect of clofazimine was due to the stimulation of mitochondrial biogenesis by peroxisome proliferator-activated receptor gamma (PPARγ). In agreement with this, clofazimine rescued mitochondrial dysfunction triggered by Htt-Q94 expression. Importantly, clofazimine also limited polyQ toxicity in developing zebrafish and neuron-specific worm models of polyQ disease.
		
		Interpretation: Our results support the potential of repurposing the antimicrobial drug clofazimine for the treatment of polyQ diseases.},
	year = {2024},
	eissn = {2352-3964},
	pages = {105124},
	orcid-numbers = {Li, Xuexin/0000-0001-5824-9720; Abbas, Anna Anoir/0000-0002-6450-2208; Pircs, Karolina Milena/0000-0001-8281-4785; Fernandez-Capetillo, Oscar/0000-0002-2690-6885}
}

@article{MTMT:34833996,
	title = {A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases},
	url = {https://m2.mtmt.hu/api/publication/34833996},
	author = {Gantsetseg, Garmaa and Bunduc, Stefania and Kói, Tamás and Hegyi, Péter and Csupor, Dezső and Dariimaa, Ganbat and Dembrovszky, Fanni and Meznerics, Fanni Adél and Ailar, Nasirzadeh and Cristina, Barbagallo and Kökény, Gábor},
	doi = {10.3390/ncrna10030030},
	journal-iso = {NON-CODING RNA},
	journal = {NON-CODING RNA},
	volume = {10},
	unique-id = {34833996},
	keywords = {[Meta-analysis]},
	year = {2024},
	eissn = {2311-553X},
	orcid-numbers = {Gantsetseg, Garmaa/0000-0001-9631-8635; Hegyi, Péter/0000-0003-0399-7259; Csupor, Dezső/0000-0002-4088-3333; Dembrovszky, Fanni/0000-0001-6953-3591; Kökény, Gábor/0000-0002-0345-6914}
}

@article{MTMT:34830464,
	title = {Budapest nephrology school - 30 years of history - from modest start to an international success: systematic summary of the 27th BNS held between 28th August and 2nd of September 2023},
	url = {https://m2.mtmt.hu/api/publication/34830464},
	author = {Cseprekál, Orsolya and Rosivall, László},
	doi = {10.1080/0886022X.2023.2282709},
	journal-iso = {RENAL FAILURE},
	journal = {RENAL FAILURE},
	volume = {46},
	unique-id = {34830464},
	issn = {0886-022X},
	abstract = {Budapest Nephrology School (BNS) could have celebrated its 30th event if it had not been interrupted by COVID pandemic for a few years. Yet, the organization of 27th BNS in August 2023 resumed its successful and traditional activities at Semmelweis University, in the beautiful central European city of Budapest. In over two decades, BNS has faithfully adapted to the changes and developments of medical science and clinical nephrology, the fact which has kept it unique and attractive for nephrologists from across the globe. With such a long history and representing the top international professors of nephrology, BNS has proved to be a successful one-week, in-person refreshing course which has attracted over 1600 medical doctors from more than 60 countries. It has well served as an academic meeting point suitable for networking and exchange of up-to-date knowledge presented by the best international experts in nephrology. The dedication and focus of these experts on education, research and patient care represent the very concept of translational medicine. The invaluable experience of the past 27 years has set the standards for BNS to contribute to the evolution of translational nephrology in Europe in the next decade.},
	keywords = {education; Budapest; nephrology; Translational medicine},
	year = {2024},
	eissn = {1525-6049},
	orcid-numbers = {Cseprekál, Orsolya/0000-0003-2867-3875; Rosivall, László/0000-0002-9809-3879}
}

@article{MTMT:34824696,
	title = {Non-adherence to cardiometabolic medication as assessed by LC-MS/MS in urine and its association with kidney and cardiovascular outcomes in type 2 diabetes mellitus},
	url = {https://m2.mtmt.hu/api/publication/34824696},
	author = {Denicolò, Sara and Reinstadler, Vera and Keller, Felix and Thöni, Stefanie and Eder, Susanne and Heerspink, Hiddo J. L. and Rosivall, László and Wiecek, Andrzej and Mark, Patrick B. and Perco, Paul and Leierer, Johannes and Kronbichler, Andreas and Oberacher, Herbert and Mayer, Gert},
	doi = {10.1007/s00125-024-06149-w},
	journal-iso = {DIABETOLOGIA},
	journal = {DIABETOLOGIA},
	volume = {Online ahead of print},
	unique-id = {34824696},
	issn = {0012-186X},
	year = {2024},
	eissn = {1432-0428},
	pages = {Online ahead of print},
	orcid-numbers = {Denicolò, Sara/0000-0002-1558-6134; Reinstadler, Vera/0000-0003-3706-2910; Keller, Felix/0000-0002-8240-7255; Heerspink, Hiddo J. L./0000-0002-3126-3730; Rosivall, László/0000-0002-9809-3879; Wiecek, Andrzej/0000-0002-8625-4188; Mark, Patrick B./0000-0003-3387-2123; Perco, Paul/0000-0003-2087-5691; Leierer, Johannes/0000-0002-7884-9827; Kronbichler, Andreas/0000-0002-2945-2946; Oberacher, Herbert/0000-0002-0963-8268; Mayer, Gert/0000-0003-4605-1789}
}

@article{MTMT:34814042,
	title = {Possible retinotoxicity of long-term vardenafil treatment},
	url = {https://m2.mtmt.hu/api/publication/34814042},
	author = {Szabó, Klaudia and Dékány, Bulcsú and Énzsöly, Anna and Hajdú, Rozina Ida and Laurik-Feuerstein, Lenke Kornélia and Szabó, Arnold and Radovits, Tamás and Mátyás, Csaba and Oláh, Attila and Kovács, Krisztián András and Szél, Ágoston and Somfai, Gábor Márk and Lukáts, Ákos},
	doi = {10.1016/j.exer.2024.109890},
	journal-iso = {EXP EYE RES},
	journal = {EXPERIMENTAL EYE RESEARCH},
	volume = {243},
	unique-id = {34814042},
	issn = {0014-4835},
	year = {2024},
	eissn = {1096-0007},
	orcid-numbers = {Dékány, Bulcsú/0000-0002-2205-8567; Énzsöly, Anna/0000-0001-6557-3940; Mátyás, Csaba/0000-0001-6095-7611; Somfai, Gábor Márk/0000-0001-6329-442X}
}

@article{MTMT:34804161,
	title = {Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages},
	url = {https://m2.mtmt.hu/api/publication/34804161},
	author = {Csiszar, Anna and Ungvári, Anna Sára and Patai, Roland and Gulej, Rafal and Yabluchanskiy, Andriy and Benyó, Zoltán and Kovács, Illés and Sótonyi, Péter and Kirkpartrick, Angelia C and Prodan, Calin I and Liotta, Eric M and Zhang, Xin A and Tóth, Péter József and Tarantini, Stefano and Sorond, Farzaneh A and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01139-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {in press},
	unique-id = {34804161},
	issn = {2509-2715},
	abstract = {Cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) are a critical but frequently underestimated aspect of cerebral small vessel disease (CSVD), bearing substantial clinical consequences. Detectable through sensitive neuroimaging techniques, CMHs reveal an extensive pathological landscape. They are prevalent in the aging population, with multiple CMHs often being observed in a given individual. CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). This review paper delves into the hypothesis that atherosclerosis, a prevalent age-related large vessel disease, extends its pathological influence into the cerebral microcirculation, thereby contributing to the development and progression of CSVD, with a specific focus on CMHs. We explore the concept of vascular aging as a continuum, bridging macrovascular pathologies like atherosclerosis with microvascular abnormalities characteristic of CSVD. We posit that the same risk factors precipitating accelerated aging in large vessels (i.e., atherogenesis), primarily through oxidative stress and inflammatory pathways, similarly instigate accelerated microvascular aging. Accelerated microvascular aging leads to increased microvascular fragility, which in turn predisposes to the formation of CMHs. The presence of hypertension and amyloid pathology further intensifies this process. We comprehensively overview the current body of evidence supporting this interconnected vascular hypothesis. Our review includes an examination of epidemiological data, which provides insights into the prevalence and impact of CMHs in the context of atherosclerosis and CSVD. Furthermore, we explore the shared mechanisms between large vessel aging, atherogenesis, microvascular aging, and CSVD, particularly focusing on how these intertwined processes contribute to the genesis of CMHs. By highlighting the role of vascular aging in the pathophysiology of CMHs, this review seeks to enhance the understanding of CSVD and its links to systemic vascular disorders. Our aim is to provide insights that could inform future therapeutic approaches and research directions in the realm of neurovascular health.},
	keywords = {ATHEROSCLEROSIS; Aging; Blood-Brain Barrier; Arteriosclerosis; stroke; Leukoaraiosis; Peripheral artery disease; VASCULAR DEMENTIA; Microbleed; White matter hyperintensities; white matter injury},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Kovács, Illés/0000-0001-5763-0482; Sótonyi, Péter/0000-0002-2216-4298; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34789637,
	title = {Water-Insoluble, Thermostable, Crosslinked Gelatin Matrix for Soft Tissue Implant Development},
	url = {https://m2.mtmt.hu/api/publication/34789637},
	author = {Varga, Viktória Dóra and Smeller, László and Várdai, Róbert and Kocsis, Bence and Zsoldos, Ibolya and Cruciani, Sara and Pala, Renzo and Hornyák, István},
	doi = {10.3390/ijms25084336},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34789637},
	issn = {1661-6596},
	abstract = {In this present study, the material science background of crosslinked gelatin (GEL) was investigated. The aim was to assess the optimal reaction parameters for the production of a water-insoluble crosslinked gelatin matrix suitable for heat sterilization. Matrices were subjected to enzymatic degradation assessments, and their ability to withstand heat sterilization was evaluated. The impact of different crosslinkers on matrix properties was analyzed. It was found that matrices crosslinked with butanediol diglycidyl ether (BDDE) and poly(ethylene glycol) diglycidyl ether (PEGDE) were resistant to enzymatic degradation and heat sterilization. Additionally, at 1 v/v % crosslinker concentration, the crosslinked weight was lower than the starting weight, suggesting simultaneous degradation and crosslinking. The crosslinked weight and swelling ratio were optimal in the case of the matrices that were crosslinked with 3% and 5% v/v BDDE and PEGDE. FTIR analysis confirmed crosslinking, and the reduction of free primary amino groups indicated effective crosslinking even at a 1% v/v crosslinker concentration. Moreover, stress–strain and compression characteristics of the 5% v/v BDDE crosslinked matrix were comparable to native gelatin. Based on material science measurements, the crosslinked matrices may be promising candidates for scaffold development, including properties such as resistance to enzymatic degradation and heat sterilization.},
	keywords = {Biomaterials; Material science; crosslinked gelatin; scaffold development},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Varga, Viktória Dóra/0009-0005-8769-1653; Hornyák, István/0000-0002-7183-8973}
}

@article{MTMT:34778269,
	title = {Heat shock factor 1 inhibition enhances the effects of modulated electro hyperthermia in a triple negative breast cancer mouse model},
	url = {https://m2.mtmt.hu/api/publication/34778269},
	author = {Leroy Viana, Pedro Henrique and Schvarcz, Csaba András and Danics, Lea and Besztercei, Balázs and Aloss, Kenan and Bokhari, Syeda Mahak Zahra and Giunashvili, Nino and Bócsi, Dániel and Koós, Zoltán and Benyó, Zoltán and Hamar, Péter},
	doi = {10.1038/s41598-024-57659-x},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {14},
	unique-id = {34778269},
	issn = {2045-2322},
	abstract = {Female breast cancer is the most diagnosed cancer worldwide. Triple negative breast cancer (TNBC) is the most aggressive type and there is no existing endocrine or targeted therapy. Modulated electro-hyperthermia (mEHT) is a non-invasive complementary cancer therapy using an electromagnetic field generated by amplitude modulated 13.56 MHz frequency that induces tumor cell destruction. However, we have demonstrated a strong induction of the heat shock response (HSR) by mEHT, which can result in thermotolerance. We hypothesized that inhibition of the heat shock factor 1 (HSF1) can synergize with mEHT and enhance tumor cell-killing. Thus, we either knocked down the HSF1 gene with a CRISPR/Cas9 lentiviral construct or inhibited HSF1 with a specific small molecule inhibitor: KRIBB11 in vivo. Wild type or HSF1-knockdown 4T1 TNBC cells were inoculated into the mammary gland’s fat pad of BALB/c mice. Four mEHT treatments were performed every second day and the tumor growth was followed by ultrasound and caliper. KRIBB11 was administrated intraperitoneally at 50 mg/kg daily for 8 days. HSF1 and Hsp70 expression were assessed. HSF1 knockdown sensitized transduced cancer cells to mEHT and reduced tumor growth. HSF1 mRNA expression was significantly reduced in the KO group when compared to the empty vector group, and consequently mEHT-induced Hsp70 mRNA upregulation diminished in the KO group. Immunohistochemistry (IHC) confirmed the inhibition of Hsp70 upregulation in mEHT HSF1-KO group. Demonstrating the translational potential of HSF1 inhibition, combined therapy of mEHT with KRIBB11 significantly reduced tumor mass compared to either monotherapy. Inhibition of Hsp70 upregulation by mEHT was also supported by qPCR and IHC. In conclusion, we suggest that mEHT-therapy combined with HSF1 inhibition can be a possible new strategy of TNBC treatment with great translational potential.},
	year = {2024},
	eissn = {2045-2322},
	orcid-numbers = {Schvarcz, Csaba András/0000-0002-2618-1909; Danics, Lea/0000-0001-8568-4074; Besztercei, Balázs/0000-0002-5636-284X; Aloss, Kenan/0000-0003-4806-7477; Giunashvili, Nino/0009-0005-2587-3806; Benyó, Zoltán/0000-0001-6015-0359; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:34775499,
	title = {Frequency of office blood pressure measurements and the seasonal variability of blood pressure: results of the Hungarian Hypertension Registry},
	url = {https://m2.mtmt.hu/api/publication/34775499},
	author = {Nemcsik, János and Takács, Johanna and Pásztor, Dorottya Tímea and Farsang, Csaba and Simon, Attila and Páll, Dénes and Torzsa, Péter and Dolgos, Szilveszter and Koller, Ákos and Habony, Norbert and Járai, Zoltán},
	doi = {10.1080/08037051.2024.2337170},
	journal-iso = {BLOOD PRESSURE},
	journal = {BLOOD PRESSURE},
	volume = {33},
	unique-id = {34775499},
	issn = {0803-7051},
	year = {2024},
	eissn = {1651-1999},
	orcid-numbers = {Nemcsik, János/0000-0002-3573-0287; Takács, Johanna/0000-0002-8709-8826; Pásztor, Dorottya Tímea/0009-0001-8399-1019; Torzsa, Péter/0000-0002-8148-4961; Koller, Ákos/0000-0003-3256-8701}
}

@article{MTMT:34773870,
	title = {Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence},
	url = {https://m2.mtmt.hu/api/publication/34773870},
	author = {Balasubramanian, Priya and Kiss, Tamás and Gulej, Rafal and Nyúl-Tóth, Ádám and Tarantini, Stefano and Yabluchanskiy, Andriy and Ungvári, Zoltán István and Csiszar, Anna},
	doi = {10.3390/nu16070952},
	journal-iso = {NUTRIENTS},
	journal = {NUTRIENTS},
	volume = {16},
	unique-id = {34773870},
	abstract = {High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mounting evidence implicating increased cellular senescence in the pathogenesis of age-related diseases. Our hypothesis posits that HFD consumption amplifies senescence burden across multiple organs. To scrutinize this hypothesis, we subjected mice to a 6-month HFD regimen, assessing senescence biomarker expression in the liver, white adipose tissue, and the brain. Aging is intrinsically linked to impaired cellular stress resilience, driven by dysfunction in Nrf2-mediated cytoprotective pathways that safeguard cells against oxidative stress-induced senescence. To ascertain whether Nrf2-mediated pathways shield against senescence induction in response to HFD consumption, we explored senescence burden in a novel model of aging: Nrf2-deficient (Nrf2+/−) mice, emulating the aging phenotype. Our initial findings unveiled significant Nrf2 dysfunction in Nrf2+/− mice, mirroring aging-related alterations. HFD led to substantial obesity, hyperglycemia, and impaired insulin sensitivity in both Nrf2+/− and Nrf2+/+ mice. In control mice, HFD primarily heightened senescence burden in white adipose tissue, evidenced by increased Cdkn2a senescence biomarker expression. In Nrf2+/− mice, HFD elicited a significant surge in senescence burden across the liver, white adipose tissue, and the brain. We postulate that HFD-induced augmentation of senescence burden may be a pivotal contributor to accelerated organismal aging and the premature onset of age-related diseases.},
	year = {2024},
	eissn = {2072-6643},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Gulej, Rafal/0000-0002-9958-707X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}