Biochemistry of Cellular Senescence

Biochemistry of Cellular Senescence

Cellular senescence is a process in which cells stop dividing and enter a state of permanent growth arrest. This phenomenon plays a crucial role in aging and age-related diseases. Senescent cells display changes in their biochemistry that distinguish them from normal proliferating cells.

Senescence-associated beta-galactosidase (SA-β-gal)

One of the most well-known markers of cellular senescence is the senescence-associated beta-galactosidase (SA-β-gal) activity. This enzyme is not present in actively proliferating cells but is upregulated in senescent cells. SA-β-gal staining is commonly used to detect senescent cells in vitro and in vivo.

P16 and P21

P16 and P21 are two key proteins that regulate cellular senescence. P16 inhibits the activity of cyclin-dependent kinases, leading to cell cycle arrest, while P21 inhibits the activity of cyclin-dependent kinases and promotes the assembly of senescence-associated heterochromatin foci (SAHF). These proteins play a crucial role in the establishment and maintenance of the senescent state.

Senescence-associated secretory phenotype (SASP)

Senescent cells secrete a variety of pro-inflammatory cytokines, chemokines, growth factors, and matrix metalloproteinases, collectively known as the senescence-associated secretory phenotype (SASP). The SASP can have both beneficial and detrimental effects, depending on the context. It can promote tissue repair and immune surveillance but can also contribute to chronic inflammation and age-related pathologies.