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1.
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
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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Saját polcon:
2.
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
Borító:
Saját polcon:
3.
001-es BibID:
BIBFORM109142
035-os BibID:
(scopus)85120642459 (wos)000729080200010
Első szerző:
Hassoun, Roua
Cím:
Do they come together? Protein quality control, stress-activated signaling, and "sarcostat" in hypertrophic cardiomyopathy progression / Hassoun Roua, Budde Heidi, Zhazykbayeva Saltanat, Herwig Melissa, Sieme Marcel, Delalat Simin, Mostafi Nusratul, Gömöri Kamilla, Tangos Melina, Jarkas Muhammad, Pabel Steffen, Bruckmüller Stefanie, Skrygan Marina, Lódi Mária, Jaquet Kornelia, Sequeira Vasco, Gambichler Thilo, Remedios Cris Dos, Kovács Árpád, Mannherz Hans Georg, Mügge Andreas, Sossalla Samuel, Hamdani Nazha
Dátum:
2022
ISSN:
0167-5273
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
levél
folyóiratcikk
Megjelenés:
International Journal Of Cardiology. - 347 (2022), p. 44-45. -
További szerzők:
Budde, Heidi
Zhazykbayeva, Saltanat
Herwig, Melissa
Sieme, Marcel
Delalat, Simin
Mostafi, Nusratul
Gömöri Kamilla
Tangos, Melina
Jarkas, Muhammad
Pabel, Steffen
Bruckmüller, Stefanie
Skrygan, Marina
Lódi Mária (1991-)
Jaquet, Kornelia
Sequeira, Vasco
Gambichler, Thilo
Remedios, Cris
Kovács Árpád (1986-) (kardiológus)
Mannherz, Hans Georg
Mügge, Andreas
Sossalla, Samuel
Hamdani, Nazha
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
4.
001-es BibID:
BIBFORM109140
035-os BibID:
(scopus)85115118583 (wos)000757375800031
Első szerző:
Hassoun, Roua
Cím:
Stress activated signalling impaired protein quality control pathways in human hypertrophic cardiomyopathy / Hassoun Roua, Budde Heidi, Zhazykbayeva Saltanat, Herwig Melissa, Sieme Marcel, Delalat Simin, Mostafi Nusratul, Gömöri Kamilla, Tangos Melina, Jarkas Muhammad, Pabel Steffen, Bruckmüller Stefanie, Skrygan Marina, Lódi Mária, Jaquet Kornelia, Sequeira Vasco, Gambichler Thilo, Remedios Cris Dos, Kovács Árpád, Mannherz Hans Georg, Mügge Andreas, Sossalla Samuel, Hamdani Nazha
Dátum:
2021
ISSN:
0167-5273
Megjegyzések:
Hypertrophic cardiomyopathy (HCM) is a complex myocardial disorder with no well-established disease-modifying therapy so far. Our study aimed to investigate how autophagy, oxidative stress, inflammation, stress signalling pathways, and apoptosis are hallmark of HCM and their contribution to the cardiac dysfunction. Demembranated cardiomyocytes from patients with HCM display increased titin-based stiffness (Fpassive), which was corrected upon antioxidant treatment. Titin as a main determinant of Fpassive was S-glutathionylated and highly ubiquitinated in HCM patients. This was associated with a shift in the balance of reduced and oxidized forms of glutathione (GSH and GSSG, respectively). Both heat shock proteins (HSP27 and ?-? crystalline) were upregulated and S-glutathionylated in HCM. Administration of HSPs in vitro significantly reduced HCM cardiomyocyte stiffness. High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM. Many regulators of signal transduction pathways that are involved in autophagy, apoptosis, cardiac contractility, and growth including the mitogen-activated protein kinase (MAPK), protein kinase B (AKT), glycogen synthase kinase 3? (GSK-3?), mammalian target of rapamycin (mTOR), forkhead box O transcription factor (FOXO), c-Jun N-terminal protein kinase (JNK), and extracellular-signal-regulated kinase (ERK1/2) were modified in HCM. The apoptotic factors cathepsin, procaspase 3, procaspase 9 and caspase 12, but not caspase 9, were elevated in HCM hearts and associated with increased proinflammatory cytokines (Interleukin 6 (IL-6), interleukin 18 (IL-18), intercellular cell adhesion molecule-1 (ICAM1), vascular cell adhesion molecule-1 (VCAM1), the Toll-like receptors 2 (TLR2) and the Toll-like receptors 4 (TLR4)) and oxidative stress (3-nitrotyrosine and hydrogen peroxide (H2O2)). Here we reveal stress signalling and impaired PQS as potential mechanisms underlying the HCM phenotype. Our data suggest that reducing oxidative stress can be a viable therapeutic approach to attenuating the severity of cardiac dysfunction in heart failure and potentially in HCM and prevent its progression.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:
International Journal Of Cardiology. - 344 (2021), p. 160-169. -
További szerzők:
Budde, Heidi
Zhazykbayeva, Saltanat
Herwig, Melissa
Sieme, Marcel
Delalat, Simin
Mostafi, Nusratul
Gömöri Kamilla
Tangos, Melina
Jarkas, Muhammad
Pabel, Steffen
Bruckmüller, Stefanie
Skrygan, Marina
Lódi Mária (1991-)
Jaquet, Kornelia
Sequeira, Vasco
Gambichler, Thilo
Remedios, Cris
Kovács Árpád (1986-) (kardiológus)
Mannherz, Hans Georg
Mügge, Andreas
Sossalla, Samuel
Hamdani, Nazha
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
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