Understanding cellular senescence: pathways involved, therapeutics and longevity aiding

A normal somatic cell undergoes cycles of finite cellular divisions. The presence of surveillance checkpoints arrests cell division in response to stress inducers: oxidative stress from excess free radicals, oncogene-induced abnormalities, genotoxic stress, and telomere attrition. When facing such stress when undergoing these damages, there is a brief pause in the cell cycle to enable repair mechanisms. Also, the nature of stress determines whether the cell goes for repair or permanent arrest. As the cells experience transient or permanent stress, they subsequently choose the quiescence or senescence stage, respectively. Quiescence is an essential stage that allows the arrested/damaged cells to go through appropriate repair mechanisms and then revert to the mainstream cell cycle. However, senescent cells are irreversible and accumulate with age, resulting in inflammation and various age-related disorders. In this review, we focus on senescence-associated pathways and therapeutics understanding cellular senescence as a cascade that leads to aging, while discussing the recent details on the molecular pathways involved in regulating senescence and the benefits of therapeutic strategies against accumulated senescent cells and their secretions.

Automated summary

Normal somatic cells undergo finite cellular divisions, but they can be arrested in response to various stressors such as oxidative stress, oncogene-induced abnormalities, genotoxic stress, and telomere attrition. Repair mechanisms are activated during the cell cycle pause caused by stress, and the nature of the stress determines whether repair or permanent arrest occurs. Quiescence allows damaged cells to repair and return to the cell cycle, while senescence is irreversible and leads to age-related disorders.