A Szentágothai János Kutatóközpont a PTE korszerű, nemzetközi tudományszervezési és menedzsment normák szerint kialakított új intézménye, amely az élettudományi, élettelen természettudományi, valamint környezettudományi oktatás...
The most important research topic of our research group is heart failure, which is the only cardiovascular disease with an increasing incidence. Heart failure is a disease characterised by poor prognosis and its mortality has not significantly reduced despite the numerous therapeutic possibilities. We also investigate the therapeutic approaches of other pathologies leading to heart failure, for example/such as myocardial infarction, hypertension and atrial fibrillation.
We are studying the role of the interplay between certain signaling factors and mitochondrial quality control in these pathological progressions. In addition, we are seeking to find possible therapeutic targets along this axis.
Based on research in recent years, the PARP enzyme is one of the most promising targets in both the prevention of heart failure and the treatment of established disease. PARP-inhibitors besides their “orthodox” NAD+-preserving effect, can also influence several signal transduction pathways. They have a direct mitochondrial protective effect, preserve the activity of the components of the respiratory chain, have a positive effect on the activity of signaling factors, thereby reducing the process of cardiovascular connective tissue remodeling.
An other promising path is the pharmacological modulation of the mitochondrial quality control. We are conducting experiments on the inhibition of fission, promoting fusion processes and enhanced the mitochondrial biogenesis, thus uncovering the role of the above mentioned processes on the development of heart failure.
DERES L, EROS K, BENCZE N, CSEKO CS, FARKAS S, SERESS L, TOTH K, HALMOSI R; THE EFFECTS OF BRADYKININ B1 RECEPTOR ANTAGONISM ON THE MYOCARDIAL AND VASCULAR CONSEQUENCES OF HYPERTENSION IN SHR RATS; FRONTIERS IN PHYSIOLOGY 21;10:624. (2019) IF:3,201
RIBA A, DERES L, SUMEGI B, TOTH K, SZABADOS E, HALMOSI R; CARDIOPROTECTIVE EFFECT OF RESVERATROL IN A POSTINFARCTION HEART FAILURE MODEL. NEW INSIGHTS INTO THE BENEFITS OF POLYPHENOLS IN CHRONIC DISEASES; OXID MED CELL LONGEV. 2017:6819281. (2017) IF: 4,593
SZABO A, SUMEGI K, FEKETE K, HOCSAK E, DEBRECENI B, SETALO G JR., KOVACS K, DERES L, KENGYEL A, KOVACS D, MANDL J, NYITRAI M, FEBBRAIO MA, GALLYAS F JR., SUMEGI B; ACTIVATION OF MITOCHONDRIAL FUSION PROVIDES A NEW TREATMENT FOR MITOCHONDRIA-RELATED DISEASES. BIOCHEM PHARMACOL. 31;150:86-96. (2018) IF: 4,581
EROS K, MAGYAR K, DERES L, RIBA A, VAMOS Z, KALLAI T, SERESS L, SUMEGI B, TOTK K, HALMOSI R; CHRONIC PARP-1 INHIBITION REDUCES CAROTID VESSEL REMODELING AND OXIDATIVE DAMAGE OF THE DORSAL HIPPOCAMPUS IN SPONTANEOUSLY HYPERTENSIVE RATS. [PLOS ONE 24;12(3):E0174401.] (2017) IF: 3,057
VOROS E, DERES L, HALMOSI R, VARADI E, TOTH K, BATTYANI I; INTERACTIONS BETWEEN IODINATED CONTRAST MEDIA AND TISSUE PLASMINOGEN ACTIVATOR: IN VITRO COMPARISON STUDY. [CLIN HEMORHEOL MICROCIRC. DOI: 10.3233/CH-170261.] (2017) IF: 1,815
RIBA A, DERES L, EROS K, SZABO A, SUMEGI B, TOTH K, HALMOSI R, SZABADOS E; DOXYCYCLINE PROTECTS AGAINST ROSINDUCED MITOCHONDRIAL FRAGMENTATION AND ISO-INDUCED HEART FAILURE [PLOS ONE 6;12(4):E0175195.] (2017) IF: 3,057
HALMOSI R1, DERES L1, GAL R, EROS K, TOTH K; PARP INHIBITION AND POSTINFARCTION MYOCARDIAL
REMODELING. INTERNATIONAL JOURNAL OF CARDIOLOGY – 2016 REVIEW INT J CARDIOL. 2016 JUN 28.
PII: S0167-5273(16)31234-7 IF: 6.189
DERES L, BARTHA E, PALFI A, EROS K, RIBA A, LANTOS J, KALAI T, HIDEG K, SUMEGI B, GALLYAS F, TOTH K, HALMOSI R; PARP-INHIBITOR TREATMENT PREVENTS HYPERTENSION INDUCED CARDIAC REMODELING BY FAVORABLE MODULATION OF HEAT SHOCK PROTEINS, AKT-1/GSK-3Β AND SEVERAL PKC ISOFORMS [PLOS ONE - PMCID: PMC4094529]. (2014) IF: 3,73
MAGYAR K, DERES L, EROS K, BRUSZT K, SERESS L, HAMAR J, HIDEG K, BALOGH A, GALLYAS F JR, SUMEGI B, TOTH K, HALMOSI R; A QUINAZOLINE-DERIVATIVE COMPOUND WITH PARP INHIBITORY EFFECT SUPPRESSES HYPERTENSION-INDUCED VASCULAR ALTERATIONS IN SPONTANEOUSLY HYPERTENSIVE RATS. BIOCHIM BIOPHYS ACTA. 19;1842(7):935-944. (2014) IF: 4.882
