Cellular Senescence: Difference between revisions

# '''Telomere Shortening''': One of the primary triggers for cellular senescence is the process of telomere attrition. Telomeres act as protective caps at the ends of chromosomes, ensuring DNA stability and integrity during cell division. However, with each division, these telomeres progressively shorten. Once they are eroded to a critical length, the cell recognizes it as a potential risk for DNA misrepair and genetic instability, leading it to enter a state of permanent growth arrest or senescence.

# '''DNA Damage''': Cells are constantly exposed to various internal and external factors that can induce DNA damage. Agents like ultraviolet radiation, environmental toxins, and metabolic by-products like reactive oxygen species can cause mutations or other DNA lesions. When the damage is too extensive or irreparable, the cell, instead of proliferating with potentially faulty DNA, enters a state of senescence to prevent the propagation of these errors.

# '''Oncogene Activation''': Oncogenes are genes that, when activated or overexpressed, can drive cells into uncontrolled growth and potentially lead to tumor formation. In certain scenarios, the activation or aberrant expression of these genes can be recognized by the cell as a precancerous signal. To counteract the risk of malignancy, the cell initiates a senescent program, effectively halting its own proliferation and thus reducing the risk of tumor development.

# Additionally, other lesser-known factors like epigenetic changes, mitochondrial dysfunction, and chronic inflammation have also been implicated in driving cells toward senescence. As research advances, our understanding of these causative factors and their interplay will pave the way for more effective therapeutic interventions targeting cellular senescence.