Ca2+/calmodulin‐dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model-Reference-Cited by-同舟云学术

Ca2+/calmodulin‐dependent protein kinase II and protein kinase G oxidation contributes to impaired sarcomeric proteins in hypertrophy model

Published:2022-05-18 Issue:4 Volume:9 Page:2585-2600
ISSN:2055-5822
Container-title:ESC Heart Failure
language:en
Short-container-title:ESC Heart Failure

Author:

Gömöri Kamilla¹²³,Herwig Melissa²⁴,Budde Heidi²⁴,Hassoun Roua²⁴,Mostafi Nusratul²⁴,Zhazykbayeva Saltanat²⁴,Sieme Marcel²⁴,Modi Suvasini²⁴,Szabados Tamara¹⁵,Pipis Judit¹⁵,Farkas‐Morvay Nikolett¹,Leprán István¹,Ágoston Gergely⁶,Baczkó István¹,Kovács Árpád²⁴,Mügge Andreas⁴,Ferdinandy Péter³⁵,Görbe Anikó¹³⁵,Bencsik Péter¹⁵,Hamdani Nazha²³⁴⁷^ORCID

Affiliation:

1. Department of Pharmacology and Pharmacotherapy University of Szeged Szeged Hungary

2. Institut für Forschung und Lehre (IFL), Molecular and Experimental Cardiology Ruhr University Bochum Bochum Germany

3. Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary

4. Department of Cardiology, St. Josef‐Hospital Ruhr University Bochum Bochum Germany

5. Pharmahungary Group Szeged Hungary

6. Institute of Family Medicine University of Szeged Szeged Hungary

7. HCEMM‐Cardiovascular Research Group, Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary

Funder

California Department of Fish and Game

Nemzeti Kutatási, Fejlesztési és Innovaciós Alap

Deutscher Akademischer Austauschdienst

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ehf2.13973

Reference78 articles.

1. Heart Plasticity in Response to Pressure- and Volume-Overload: A Review of Findings in Compensated and Decompensated Phenotypes

2. NADPH oxidase-4 promotes eccentric cardiac hypertrophy in response to volume overload

3. Myocardial Structure and Function Differ in Systolic and Diastolic Heart Failure

4. The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress in cardiovascular diseases

5. CALCIUM, THIN FILAMENTS, AND THE INTEGRATIVE BIOLOGY OF CARDIAC CONTRACTILITY

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