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001-es BibID:	BIBFORM129740
035-os BibID:	(WoS)001442711800001
Első szerző:	Bódi Beáta (molekuláris biológus)
Cím:	Differential Myocardial Responses in Male and Female Rats with Uremic Cardiomyopathy / Beáta Bódi, Rebeka Rita Vágó, László Nagy, Arnold Péter Ráduly, András Gulyás, Klaudia Kupecz, Lilian Azar, Fanni Magdolna Márványkövi, Gergő Szűcs, Andrea Siska, Gábor Cserni, Imre Földesi, Zoltán Papp, Márta Sárközy
Dátum:	2025
ISSN:	1661-6596 1422-0067
Megjegyzések:	Uremic cardiomyopathy, characterized by diastolic dysfunction, left ventricular hypertrophy (LVH), and fibrosis, is a common cardiovascular complication of chronic kidney disease (CKD). Men are at a higher risk for cardiovascular and renal diseases, compared to age-matched, pre-menopausal women. We aimed to investigate the influence of sex on the severity of uremic cardiomyopathy through the characterization of functional and molecular indices of myocardial remodeling in a rat model. CKD was induced by a 5/6 nephrectomy in 9-week-old male and female Wistar rats. Serum and urine tests, transthoracic echocardiography, left ventricular (LV) histology, and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were performed at week 8 or 9. Moreover, LV alterations were also tested in permeabilized cardiomyocytes (CMs) by force measurements and Western immunoblotting. CKD resulted in the development of a more severe uremic cardiomyopathy in male rats-including LVH, LV diastolic dysfunction, and fibrosis-than in female rats, where only LVH was observed. A uremic cardiomyopathy was also associated with a decrease in maximal Ca2+-activated force (Fmax) in CMs of male rats. Additionally, increases in CM Ca2+-independent passive stiffness (Fpassive) and decreases in cardiac myosin-binding protein C (cMyBP-C) phosphorylation levels were significantly larger in male than female rats. In conclusion, a uremic cardiomyopathy involved cardiac remodeling in both sexes. Nevertheless, male rats exhibited more pronounced signs of macroscopic and microscopic alterations than their female counterparts, illustrating a sex-dependent component of uremic cardiomyopathy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk active force diastolic dysfunction left ventricular hypertrophy passive stiffness permeabilized cardiomyocyte uremic cardiomyopathy
Megjelenés:	International Journal Of Molecular Sciences. - 26 : 5 (2025), p. 1-20. -
További szerzők:	Vágó Rebeka Rita Nagy László (1988-) (orvos) Ráduly Arnold Péter (1993-) Gulyás András Kupecz Klaudia Azar Lilian Márványkövi Fanni Magdolna Szűcs Gergő Siska Andrea Cserni Gábor Földesi Imre Papp Zoltán (1965-) (kardiológus, élettanász) Sárközy Márta
Pályázati támogatás:	GINOP-2.3.2-15-2016-00040 GINOP EFOP-3.6.2-16-2017-00006 EFOP NKFIH FK129094 Egyéb EKÖP-24-2-de-167 Egyéb
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001-es BibID:	BIBFORM097205
035-os BibID:	(scopus)85116968958 (wos)000716921300001
Első szerző:	Bódi Beáta (molekuláris biológus)
Cím:	Alterations in ACE and ACE2 Activities and Cardiomyocyte Signaling Underlie Improved Myocardial Function in a Rat Model of Repeated Remote Ischemic Conditioning / Beáta Bódi, Patrick M. Pilz, Lilla Mártha, Miriam Lang, Ouafa Hamza, Miklós Fagyas, Petra L. Szabó, Dietmar Abraham, Attila Tóth, Bruno K. Podesser, Attila Kiss, Zoltán Papp
Dátum:	2021
ISSN:	1661-6596 1422-0067
Megjegyzések:	Post-ischemic left ventricular (LV) remodeling and its hypothetical prevention by repeated remote ischemic conditioning (rRIC) in male Sprague?Dawley rats were studied. Myocardial infarction (MI) was evoked by permanent ligation of the left anterior descending coronary artery (LAD), and myocardial characteristics were tested in the infarcted anterior and non-infarcted inferior LV re-gions four and/or six weeks later. rRIC was induced by three cycles of five-minute-long unilateral hind limb ischemia and five minutes of reperfusion on a daily basis for a period of two weeks starting four weeks after LAD occlusion. Sham operated animals served as controls. Echocardio-graphic examinations and invasive hemodynamic measurements revealed distinct changes in LV systolic function between four and six weeks after MI induction in the absence of rRIC (i.e., LV ejection fraction (LVEF) decreased from 52.8 ? 2.1% to 50 ? 1.6%, mean ? SEM, p < 0.05) and in the presence of rRIC (i.e., LVEF increased from 48.2 ? 4.8% to 55.2 ? 4.1%, p < 0.05). Angioten-sin-converting enzyme (ACE) activity was about five times higher in the anterior LV wall at six weeks than that in sham animals. Angiotensin-converting enzyme 2 (ACE2) activity roughly doubled in post-ischemic LVs. These increases in ACE and ACE2 activities were effectively miti-gated by rRIC. Ca2+-sensitivities of force production (pCa50) of LV permeabilized cardiomyocytes were increased at six weeks after MI induction together with hypophosphorylation of 1) cardiac troponin I (cTnI) in both LV regions, and 2) cardiac myosin-binding protein C (cMyBP-C) in the anterior wall. rRIC normalized pCa50, cTnI and cMyBP-C phosphorylations. Taken together, post-ischemic LV remodeling involves region-specific alterations in ACE and ACE2 activities to-gether with changes in cardiomyocyte myofilament protein phosphorylation and function. rRIC has the potential to prevent these alterations and to improve LV performance following MI.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk repeated remote ischemic conditioning cardiomyocyte mechanics signaling
Megjelenés:	International Journal Of Molecular Sciences. - 22 : 20 (2021), p. 1-17. -
További szerzők:	Pilz, Patrick M. Mártha Lilla Lang, Miriam Hamza, Ouafa Fagyas Miklós (1984-) (orvos) Szabó Petra Lujza Abraham, Dietmar Tóth Attila (1971-) (biológus) Podesser, Bruno Karl Kiss Attila Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP Austria-Hungary Action Foundation: 92öu8 Egyéb Ludwig Boltzmann Society: REM2017-20 Egyéb 2020-4.1.1-TKP2020 Egyéb TKP2020-IKA-04 Egyéb TKP2020-NKA04 Egyéb FK 128809 OTKA K 132623 OTKA COST Action EU-CARDIOPROTECTION: CA16225 Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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