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001-es BibID:BIBFORM109146
035-os BibID:(cikkazonosító)2210 (scopus)85141789638 (wos)000883366200001
Első szerző:Gömöri Kamilla
Cím:Altered Cellular Protein Quality Control System Modulates Cardiomyocyte Function in Volume Overload-Induced Hypertrophy / Gömöri Kamilla, Herwig Melissa, Hassoun Roua, Budde Heidi, Mostafi Nusratul, Delalat Simin, Modi Suvasini, Begovic Merima, Szabados Tamara, Pipis Judit, Farkas-Morvay Nikolett, Leprán István, Kovács Árpád, Mügge Andreas, Ferdinandy Péter, Görbe Anikó, Bencsik Péter, Hamdani Nazha
Dátum:2022
ISSN:2076-3921
Megjegyzések:Volume-induced hypertrophy is one of the risk factors for cardiac morbidity and mortality. In addition, mechanical and metabolic dysfunction, aging, and cellular redox balance are also contributing factors to the disease progression. In this study, we used volume overload (VO), which was induced by an aortocaval fistula in 2-month-old male Wistar rats, and sham-operated animals served as control. Functional parameters were measured by transthoracic echocardiography at termination 4- or 8-months after VO. The animals showed hypertrophic remodeling that was accompanied by mechanical dysfunction and increased cardiomyocyte stiffness. These alterations were reversible upon treatment with glutathione. Cardiomyocyte dysfunction was associated with elevated oxidative stress markers with unchanged inflammatory signaling pathways. In addition, we observed altered phosphorylation status of small heat shock proteins 27 and 70 and diminished protease expression caspases 3 compared to the matched control group, indicating an impaired protein quality control system. Such alterations might be attributed to the increased oxidative stress as anticipated from the enhanced titin oxidation, ubiquitination, and the elevation in oxidative stress markers. Our study showed an early pathological response to VO, which manifests in cardiomyocyte mechanical dysfunction and dysregulated signaling pathways associated with enhanced oxidative stress and an impaired protein quality control system.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Antioxidants. - 11 : 11 (2022), p. 1-16. -
További szerzők:Herwig, Melissa Hassoun, Roua Budde, Heidi Mostafi, Nusratul Delalat, Simin Modi, Suvasini Begovic, Merima Szabados Tamara Pipis Judit Farkas-Morvay Nikolett Leprán István Kovács Árpád (1986-) (kardiológus) Mügge, Andreas Ferdinándy Péter Görbe Anikó Bencsik Péter Hamdani, Nazha
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001-es BibID:BIBFORM109145
035-os BibID:(scopus)85130294773 (wos)000797144600001
Első szerző:Gömöri Kamilla
Cím:Ca2+/calmodulin-dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model / Gömöri Kamilla, Herwig Melissa, Budde Heidi, Hassoun Roua, Mostafi Nusratul, Zhazykbayeva Saltanat, Sieme Marcel, Modi Suvasini, Szabados Tamara, Pipis Judit, Farkas-Morvay Nikolett, Leprán István, Ágoston Gergely, Baczkó István, Kovács Árpád, Mügge Andreas, Ferdinandy Péter, Görbe Anikó, Bencsik Péter, Hamdani Nazha
Dátum:2022
ISSN:2055-5822
Megjegyzések:Aims: Volume overload (VO) induced hypertrophy is one of the hallmarks to the development of heart diseases. Understanding the compensatory mechanisms involved in this process might help preventing the disease progression. Methods and results: Therefore, the present study used 2 months old Wistar rats, which underwent an aortocaval fistula to develop VO-induced hypertrophy. The animals were subdivided into four different groups, two sham operated animals served as age-matched controls and two groups with aortocaval fistula. Echocardiography was performed prior termination after 4- and 8-month. Functional and molecular changes of several sarcomeric proteins and their signalling pathways involved in the regulation and modulation of cardiomyocyte function were investigated. Results: The model was characterized with preserved ejection fraction in all groups and with elevated heart/body weight ratio, left/right ventricular and atrial weight at 4- and 8-month, which indicates VO-induced hypertrophy. In addition, 8-months groups showed increased left ventricular internal diameter during diastole, RV internal diameter, stroke volume and velocity-time index compared with their age-matched controls. These changes were accompanied by increased Ca2+ sensitivity and titin-based cardiomyocyte stiffness in 8-month VO rats compared with other groups. The altered cardiomyocyte mechanics was associated with phosphorylation deficit of sarcomeric proteins cardiac troponin I, myosin binding protein C and titin, also accompanied with impaired signalling pathways involved in phosphorylation of these sarcomeric proteins in 8-month VO rats compared with age-matched control group. Impaired protein phosphorylation status and dysregulated signalling pathways were associated with significant alterations in the oxidative status of both kinases CaMKII and PKG explaining by this the elevated Ca2+ sensitivity and titin-based cardiomyocyte stiffness and perhaps the development of hypertrophy. Conclusions: Our findings showed VO-induced cardiomyocyte dysfunction via deranged phosphorylation of myofilament proteins and signalling pathways due to increased oxidative state of CaMKII and PKG and this might contribute to the development of hypertrophy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:ESC heart failure. - 9 : 4 (2022), p. 2585-2600. -
További szerzők:Herwig, Melissa Budde, Heidi Hassoun, Roua Mostafi, Nusratul Zhazykbayeva, Saltanat Sieme, Marcel Modi, Suvasini Szabados Tamara Pipis Judit Farkas-Morvay Nikolett Leprán István Ágoston Gergely Baczkó István Kovács Árpád (1986-) (kardiológus) Mügge, Andreas Ferdinándy Péter Görbe Anikó Bencsik Péter Hamdani, Nazha
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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