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1.

001-es BibID:BIBFORM109143
035-os BibID:(cikkazonosító)928232 (scopus)85134501154 (wos)000829869500001
Első szerző:Budde, Heidi
Cím:Current Understanding of Molecular Pathophysiology of Heart Failure With Preserved Ejection Fraction / Budde Heidi, Hassoun Roua, Mügge Andreas, Kovács Árpád, Hamdani Nazha
Dátum:2022
ISSN:1664-042X
Megjegyzések:Heart Failure (HF) is the most common cause of hospitalization in the Western societies. HF is a heterogeneous and complex syndrome that may result from any dysfunction of systolic or diastolic capacity. Abnormal diastolic left ventricular function with impaired relaxation and increased diastolic stiffness is characteristic of heart failure with preserved ejection fraction (HFpEF). HFpEF accounts for more than 50% of all cases of HF. The prevalence increases with age: from around 1% for those aged <55 years to >10% in those aged 70 years or over. Nearly 50% of HF patients have HFrEF and the other 50% have HFpEF/HFmrEF, mainly based on studies in hospitalized patients. The ESC Long-Term Registry, in the outpatient setting, reports that 60% have HFrEF, 24% have HFmrEF, and 16% have HFpEF. To some extent, more than 50% of HF patients are female. HFpEF is closely associated with co-morbidities, age, and gender. Epidemiological evidence suggests that HFpEF is highly represented in older obese women and proposed as 'obese female HFpEF phenotype'. While HFrEF phenotype is more a male phenotype. In addition, metabolic abnormalities and hemodynamic perturbations in obese HFpEF patients appear to have a greater impact in women then in men (Sorimachi et al., European J of Heart Fail, 2022, 22). To date, numerous clinical trials of HFpEF treatments have produced disappointing results. This outcome suggests that a "one size fits all" approach to HFpEF may be inappropriate and supports the use of tailored, personalized therapeutic strategies with specific treatments for distinct HFpEF phenotypes. The most important mediators of diastolic stiffness are the cardiomyocytes, endothelial cells, and extracellular matrix (ECM). The complex physiological signal transduction networks that respond to the dual challenges of inflammatory and oxidative stress are major factors that promote the development of HFpEF pathologies. These signalling networks contribute to the development of the diseases. Inhibition and/or attenuation of these signalling networks also delays the onset of disease. In this review, we discuss the molecular mechanisms associated with the physiological responses to inflammation and oxidative stress and emphasize the nature of the contribution of most important cells to the development of HFpEF via increased inflammation and oxidative stress.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Physiology. - 13 (2022), p. 1-18. -
További szerzők:Hassoun, Roua Mügge, Andreas Kovács Árpád (1986-) (kardiológus) Hamdani, Nazha
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2.

001-es BibID:BIBFORM109139
035-os BibID:(cikkazonosító)1134 (scopus)85110167526 (wos)000675938200001
Első szerző:Budde, Heidi
Cím:The Interplay between S-Glutathionylation and Phosphorylation of Cardiac Troponin I and Myosin Binding Protein C in End-Stage Human Failing Hearts / Budde Heidi, Hassoun Roua, Tangos Melina, Zhazykbayeva Saltanat, Herwig Melissa, Varatnitskaya Marharyta, Sieme Marcel, Delalat Simin, Sultana Innas, Kolijn Detmar, Gömöri Kamilla, Jarkas Muhammad, Lódi Mária, Jaquet Kornelia, Kovács Árpád, Mannherz Hans Georg, Sequeira Vasco, Mügge Andreas, Leichert Lars I., Sossalla Samuel, Hamdani Nazha
Dátum:2021
ISSN:2076-3921
Megjegyzések:Oxidative stress is defined as an imbalance between the antioxidant defense system and the production of reactive oxygen species (ROS). At low levels, ROS are involved in the regulation of redox signaling for cell protection. However, upon chronical increase in oxidative stress, cell damage occurs, due to protein, DNA and lipid oxidation. Here, we investigated the oxidative modifications of myofilament proteins, and their role in modulating cardiomyocyte function in end-stage human failing hearts. We found altered maximum Ca2+-activated tension and Ca2+ sensitivity of force production of skinned single cardiomyocytes in end-stage human failing hearts compared to non-failing hearts, which was corrected upon treatment with reduced glutathione enzyme. This was accompanied by the increased oxidation of troponin I and myosin binding protein C, and decreased levels of protein kinases A (PKA)- and C (PKC)-mediated phosphorylation of both proteins. The Ca2+ sensitivity and maximal tension correlated strongly with the myofilament oxidation levels, hypo-phosphorylation, and oxidative stress parameters that were measured in all the samples. Furthermore, we detected elevated titin-based myocardial stiffness in HF myocytes, which was reversed by PKA and reduced glutathione enzyme treatment. Finally, many oxidative stress and inflammation parameters were significantly elevated in failing hearts compared to non-failing hearts, and corrected upon treatment with the anti-oxidant GSH enzyme. Here, we provide evidence that the altered mechanical properties of failing human cardiomyocytes are partially due to phosphorylation, S-glutathionylation, and the interplay between the two post-translational modifications, which contribute to the development of heart failure.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Antioxidants. - 10 : 7 (2021), p. 1-26. -
További szerzők:Hassoun, Roua Tangos, Melina Zhazykbayeva, Saltanat Herwig, Melissa Varatnitskaya, Marharyta Sieme, Marcel Delalat, Simin Sultana, Innas Kolijn, Detmar Gömöri Kamilla Jarkas, Muhammad Lódi Mária (1991-) Jaquet, Kornelia Kovács Árpád (1986-) (kardiológus) Mannherz, Hans Georg Sequeira, Vasco Mügge, Andreas Leichert, Lars I. Sossalla, Samuel Hamdani, Nazha
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

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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Intézményi repozitóriumban (DEA) tárolt változat
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4.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM095255
Első szerző:Kovács Árpád (kardiológus)
Cím:Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart / Árpád Kovács, Melissa Herwig, Heidi Budde, Simin Delalat, Detmar Kolijn, Beáta Bódi, Roua Hassoun, Melina Tangos, Saltanat Zhazykbayeva, Ágnes Balogh, Dániel Czuriga, Sophie Van Linthout, Carsten Tschöpe, Naranjan S. Dhalla, Andreas Mügge, Attila Tóth, Zoltán Papp, Judit Barta, Nazha Hamdani
Dátum:2021
ISSN:2076-3921
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Antioxidants. - 10 : 6 (2021), p. 1-21. -
További szerzők:Herwig, Melissa Budde, Heidi Delalat, Simin Kolijn, Detmar Bódi Beáta (1989-) (molekuláris biológus) Hassoun, Roua Tangos, Melina Zhazykbayeva, Saltanat Balogh Ágnes (1984-) (kardiológus) Czuriga Dániel (1982-) (kardiológus) Linthout, Sophie Van Tschöpe, Carsten Dhalla, Naranjan S. Mügge, Andreas Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Barta Judit (1975-) (kardiológus) Hamdani, Nazha
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Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM102227
035-os BibID:(WoS)000879481000020 (Scopus)85131795534
Első szerző:Tangos, Melina
Cím:SARS-CoV-2 infects human cardiac myocytes promoted by inflammation and oxidative stress / Tangos Melina, Budde Heidi, Kolijn Detmar, Sieme Marcel, Zhazykbayeva Saltanat, Lódi Mária, Herwig Melissa, Gömöri Kamilla, Hassoun Roua, Robinson Emma Louise, Meister Toni Luise, Jaquet Kornelia, Kovács Árpád, Mustroph Julian, Evert Katja, Babel Nina, Miklós Fagyas, Lindner Diana, Püschel Klaus, Westermann Dirk, Mannherz Hans Georg, Paneni Francesco, Pfaender Stephanie, Toth Attila, Mügge Andreas, Sossalla Samuel, Hamdani Nazha
Dátum:2022
ISSN:0167-5273
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:International Journal Of Cardiology. - 362 (2022), p. 196-205. -
További szerzők:Budde, Heidi Kolijn, Detmar Sieme, Marcel Zhazykbayeva, Saltanat Lódi Mária (1991-) Herwig, Melissa Gömöri Kamilla Hassoun, Roua Robinson, Emma Louise Meister, Toni Luise Jaquet, Kornelia Kovács Árpád (1986-) (kardiológus) Mustroph, Julian Evert, Katja Babel, Nina Fagyas Miklós (1984-) (orvos) Lindner, Diana Püschel, Klaus Westermann, Dirk Mannherz, Hans Georg Paneni, Francesco Pfaender, Stephanie Tóth Attila (1971-) (biológus) Mügge, Andreas Sossalla, Samuel Hamdani, Nazha
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Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM112630
035-os BibID:(cikkazonosító)1157398 (WoS)001012439700001 (Scopus)85163146346
Első szerző:Zhazykbayeva, Saltanat
Cím:Oxidative stress and inflammation distinctly drive molecular mechanisms of diastolic dysfunction and remodeling in female and male heart failure with preserved ejection fraction rats / Zhazykbayeva Saltanat, Hassoun Roua, Herwig Melissa, Budde Heidi, Kovács Árpád, Mannherz Hans Georg, El-Battrawy Ibrahim, Tóth Attila, Schmidt Wolfgang E., Mügge Andreas, Hamdani Nazha
Dátum:2023
ISSN:2297-055X
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Cardiovascular Medicine. - 10 (2023), p. 1-14. -
További szerzők:Hassoun, Roua Herwig, Melissa Budde, Heidi Kovács Árpád (1986-) (kardiológus) Mannherz, Hans Georg El-Battrawy, Ibrahim Tóth Attila (1971-) (biológus) Schmidt, Wolfgang Mügge, Andreas Hamdani, Nazha
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Intézményi repozitóriumban (DEA) tárolt változat
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