Figure 1.

DNA damage, telomeric erosions, and mitochondrial dysfunction culminate in cellular damage that favors the cellular senescence process, mediated by increased beta-galactosidase activity, the expression of p53, p16, and p21, and the secretion of a SASP observed by the expression of IL1α, IL1β, MCP1, and TNFα. These cellular damages favor pro-aging changes, such as increased damage and inflammation, reduced repair, clearance, cell renewal, and tissue function, causing effects on adjacent tissues and the exhaustion of stem cells.