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H2S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence
- Source :
- Archives of Physiology and Biochemistry. :1-14
- Publication Year :
- 2021
- Publisher :
- Informa UK Limited, 2021.
-
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.
- 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
Subjects
Details
- ISSN :
- 17444160 and 13813455
- Database :
- OpenAIRE
- Journal :
- Archives of Physiology and Biochemistry
- Accession number :
- edsair.doi...........a447411bb8c9fd721911d92c045b1bdb