Apoptosis and senescence regulatory networks

Apoptosis and senescence regulatory networks are integrated signaling systems that determine whether a cell undergoes programmed death or enters a state of permanent growth arrest in response to cellular stress (PubMed: 31036898). Apoptosis is a highly regulated process of cell suicide essential for development and the elimination of damaged cells, while senescence serves as a potent anti-tumor mechanism by preventing the replication of cells with genomic instability (NIH: PMC5744394). These pathways are interconnected through shared molecular nodes such as p53, p21, and the BCL-2 protein family, which balance survival and death signals (PubMed: 23426265). Dysregulation of these networks is a hallmark of cancer, where cells evade apoptosis, and aging, where the accumulation of senescent cells promotes chronic inflammation via the senescence-associated secretory phenotype (SASP) (PubMed: 29559598). Pharmacological intervention focuses on 'senolytics' to clear senescent cells and 'pro-apoptotic' agents to restore death pathways in malignant cells, offering therapeutic potential for oncology and age-related degenerative conditions (PubMed: 32679744).

Other names

Programmed cell death and cellular senescence pathwaysApoptosis-senescence axisCell fate regulatory networks

Modulation of pro- and anti-apoptotic proteins (e.g., BCL-2 family) to induce programmed cell death or eliminate senescent cells (senolysis) (PubMed: 32679744).