The Yin and Yang of cellular senescence in ischemia-induced myocardial injury

Cellular senescence is a stress responsive program that critically affects chronological and biological aging, ischemia reperfusion injury (IRI), and age related cardiovascular diseases. Of relevance, cardiac senescent cells exhibit altered characteristics that promote inflammation, remodeling, and fibrosis, ultimately contributing to the functional decline following myocardial infarction (MI). At the same time, emerging evidence suggests that senescence may also exert protective effects post-MI, limiting fibrosis. Thus, understanding the mechanisms and pathways of cardiac senescence appears critical for delineating the consequences of IRI, including identification of novel therapeutic targets for improving post-MI recovery.