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Figure 1. Cardiomyocyte senescence. Upstream stressors such as aging, ischemia, ischemia/reperfusion, and doxorubicin activate the DNA damage response/p53 and p16 signaling, which in turn leads to cardiomyocyte senescence. Senescent cardiomyocytes feature enlarged cell size, increased levels of p16, p21, and γH2AX, increased senescence-associated β-galactosidase (SA-β-gal) activity, and the senescence-associated secretory phenotype (SASP). The accumulation of senescent cardiomyocytes in the heart results in cardiac hypertrophy, fibrosis, and dysfunction. The figure was generated with BioRender.com.