Inhibiting the Hif-1α-Drp1 axis alleviates mitochondrial dysfunction and reduces senescence-like changes in myocardial tissue after acute myocardial infarction.
Abstract
Cellular senescence is a significant pathological process in acute myocardial infarction (AMI), yet its upstream regulatory mechanisms remain unclear. This study reveals that the HIF-1α /Drp1 signaling axis serves as a critical link between hypoxia and senescence-like changes in myocardial tissue by disrupting mitochondrial homeostasis.
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Research summary
Inhibiting the HIF-1α-Drp1 axis can alleviate mitochondrial dysfunction and reduce senescence-like changes in myocardial tissue after acute myocardial infarction. This research addresses a potential upstream mechanism of cellular senescence, which is a key factor in aging and age-related diseases, thus contributing to the understanding of longevity.
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