Endogenous sulfur dioxide deficiency as a driver of cardiomyocyte senescence through abolishing sulphenylation of STAT3 at cysteine 259.

ABSTRACT:

Objective

Cardiomyocyte senescence is an important contributor to cardiovascular diseases and can be induced by stressors including DNA damage, oxidative stress, mitochondrial dysfunction, epigenetic regulation, etc. However, the underlying mechanisms for the development of cardiomyocyte senescence remain largely unknown. Sulfur dioxide (SO₂) is produced endogenously by aspartate aminotransferase 2 (AAT2) catalysis and plays an important regulatory role in the development of cardiovascular diseases. The present study aimed to explore the effect of endogenous SO₂ on cardiomyocyte senescence and the underlying molecular mechanisms.

Approach and results

We interestingly found a substantial reduction in the expression of AAT2 in the heart of aged mice in co

SUBMITTER: Zhang S 

PROVIDER: S-EPMC10963856 | biostudies-literature | 2024 May

REPOSITORIES: biostudies-literature