Cardiomyocyte apoptosis

Cardiomyocyte apoptosis refers to the genetically regulated form of programmed cell death occurring within heart muscle cells. It plays an essential role both in normal heart development and pathological conditions such as heart failure and ischemic injury. The process involves two main pathways—the intrinsic mitochondrial pathway and extrinsic receptor-mediated pathway—both converging on activation of caspases that execute cellular demolition. Excessive or dysregulated cardiomyocyte apoptosis contributes significantly to loss of contractile tissue mass seen in various cardiovascular diseases including dilated cardiomyopathy and post-infarction remodeling. While numerous molecular players have been identified—including members of the Bcl‑2 protein family, cytochrome c release mechanisms, caspases, and surface “death” receptors—no single molecule defines this complex biological event; thus “cardiomyocyte apoptosis” should be considered an outcome/process rather than a discrete druggable target.[1][4][5]

Other names

Cardiac myocyte apoptosisMyocardial cell apoptosisApoptotic cardiomyocyte death

Drugs act by inhibiting caspase activation/executioner function; modulating mitochondrial membrane permeability via Bcl‑2 family proteins; and blocking extrinsic apoptotic signaling through death receptors like Fas/CD95.