1. H2S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence
- Author
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Guangdong Yang, Ruihuan Yu, Yuehong Wang, and Jiechun Zhu
- Subjects
Senescence ,Physiology ,medicine.disease_cause ,Lipid peroxidation ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Physiology (medical) ,medicine ,Viability assay ,030304 developmental biology ,0303 health sciences ,biology ,Chemistry ,Cystathionine gamma-lyase ,General Medicine ,equipment and supplies ,Cystathionine beta synthase ,3. Good health ,Cell biology ,Lipotoxicity ,biology.protein ,lipids (amino acids, peptides, and proteins) ,030217 neurology & neurosurgery ,Intracellular ,Oxidative stress - Abstract
Hydrogen sulphide (H2S), a newly identified gasotransmitter, can be endogenously produced by cystathionine gamma-lyase (CSE) in the cardiovascular system. This study investigated the role of the CSE/H2S system on lipid overload-induced lipotoxicity and cardiac senescence. Lipid overload in rat cardiomyocyte cells (H9C2) promoted intracellular accumulation of lipid, oxidative stress, mitochondrial dysfunctions, lipid peroxidation and inhibited cell viability, all of which could be reversed by exogenously applied H2S. Further data revealed that H2S protected H9C2 cells from lipid overload-induced senescence by altering the expressions of lipid metabolism-related genes and inhibiting cellular acetyl-CoA and global protein acetylation. Enhancement of protein acetylation abolished the protective role of H2S on cardiac senescence. In vivo, knockout of the CSE gene strengthened cardiac lipid accumulation, protein acetylation, and cellular ageing in high fat diet-fed mice. Taken together, the CSE/H2S system is capable of maintaining lipid homeostasis and cellular senescence in heart cells under lipid overload.
- Published
- 2021