S100A1’s single cysteine is an indispensable redox switch for the protection against diastolic calcium waves in cardiomyocytes-Reference-Cited by-同舟云学术

S100A1’s single cysteine is an indispensable redox switch for the protection against diastolic calcium waves in cardiomyocytes

Published:2024-07-01 Issue:1 Volume:327 Page:H275-H286
ISSN:0363-6135
Container-title:American Journal of Physiology-Heart and Circulatory Physiology
language:en
Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology

Author:

Seitz Andreas¹²,Busch Martin¹,Kroemer Jasmin¹,Schneider Andrea¹,Simon Stephanie¹,Jungmann Andreas¹³,Katus Hugo A.³⁴,Most Patrick¹³⁵⁶,Ritterhoff Julia¹³⁵^ORCID

Affiliation:

1. Molecular and Translational Cardiology, Department of Internal Medicine III, Heidelberg University Hospital, Heidelberg, Germany

2. Department of Cardiology and Angiology, Robert-Bosch-Krankenhaus, Stuttgart, Germany

3. German Centre for Cardiovascular Research (DZHK), partner site Heidelberg/Mannheim, Heidelberg, Germany

4. Department of Internal Medicine III, Heidelberg University Hospital, Heidelberg, Germany

5. Informatics for Life consortium, Klaus Tschira Foundation, Heidelberg, Germany

6. Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, United States

Abstract

S100A1 is an emerging candidate for future gene-therapy treatment of human chronic heart failure. We aimed to study the significance of the conserved single-cysteine 85 (C85) residue in cardiomyocytes. We show that S100A1 is endogenously glutathionylated in the heart and demonstrate that this is dispensable to increase systolic Ca2+ transients, but indispensable for mediating S100A1’s protection against sarcoplasmic reticulum (SR) Ca2+ waves, which was dependent on the ryanodine receptor 2 (RyR2) nitrosylation status.

Funder

Deutsches Zentrum für Herz-Kreislaufforschung

Klaus Tschira Stiftung

Publisher

American Physiological Society

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpheart.00634.2023

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