Cellular senescence

Cellular senescence is a durable state in which a cell stops dividing while remaining metabolically active. Senescent cells often alter their secretions and influence nearby cells.

p53: A tumor-suppressor protein that responds to cellular stress by regulating genes involved in cell-cycle arrest, DNA repair, and cell death. DNA damage can activate p53, which helps impose senescence by stopping the cell cycle.
Cell cycle arrest: A temporary or lasting halt in progression through the stages of cell division. Senescence is a durable form of cell-cycle arrest, not merely a short pause.
Tumor suppression: The prevention or limitation of cancer through mechanisms that restrain abnormal cell growth. Senescence can prevent damaged or oncogene-activated cells from proliferating.
Leonard Hayflick: An American anatomist who showed that normal human cells divide only a limited number of times in culture. His experiments established the finite replicative lifespan associated with cellular senescence.
Senolytics: Drugs designed to selectively eliminate senescent cells by exploiting their survival dependencies. Their development tests whether removing accumulated senescent cells can improve health.
p16INK4a: A cyclin-dependent kinase inhibitor encoded by CDKN2A that restrains cell-cycle progression through the retinoblastoma protein. Its increased expression can maintain the durable growth arrest characteristic of senescence.
Telomere: A repetitive DNA-protein structure that protects the ends of linear chromosomes. Progressive telomere shortening can trigger replicative senescence in dividing cells.
Wound healing: The coordinated biological process that repairs damaged tissue and restores its structure and function. Transient senescent cells can release signals that support aspects of tissue repair.
Paul Moorhead: A cytogeneticist who collaborated with Leonard Hayflick on studies of finite cell division in human fibroblasts. Their work helped distinguish normal-cell growth limits from continuous growth in cancer-derived cultures.
Senomorphics: Treatments intended to alter harmful features of senescent cells without killing them. They target damaging secretions while seeking to preserve senescence’s protective effects.

Linked from 28 pages