Senescence

Genetic programming aging theories posit that the DNA genetic code comprises a built-in time limit for human cell reproduction. Such theories claim that cells stop dividing after a particular time or become harmful to one’s body (Feldman, 2018). On the other hand, the wear-and-tear theories posit that the body’s mechanical functions work less efficiently as individuals age. Senescence is a cellular reaction characterized by a stable growth arrest and other phenotypic alterations comprising a proinflammatory secretome (McHugh & Gil, 2018). Senescence plays a crucial role in normal development, limits tumor progression, and maintains the homeostasis of tissues. However, it has also been linked with many common diseases as individuals age.

There is a close link between senescence and other antagonistic aging hallmarks. For instance, senescent cells display reduced mitophagy, leading to an old or defective mitochondrial network that might play a role in metabolic dysfunction as individuals age (McHugh & Gil, 2018). The integrative aging hallmarks are also influenced by aging. When stem cells are exhausted as individuals age, there is a reduction in functionality and renewal capacity, which then causes tissue deterioration. This decline is associated with increased senescent hematopoietic stem cells and reduced immunity, exposing older adults to many diseases. Furthermore, age-related pathologies like osteoporosis, sarcopenia, and osteoarthritis are also linked with senescence markers.

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Senescence is majorly driven by factors such as telomere damage (which quickens the process of aging), metabolic dysfunction (caloric restriction can impede aging decline), and pathways that regulate the senescence growth arrest. According to McHugh and Gil (2018), the induction of stable growth arrest is considered the defining characteristic of senescence. Furthermore, it is paramount to have a stable arrest to halt the propagation of dysfunctional cells. Senescent cells play a vital role in the development of diseases like cardiovascular diseases, osteoporosis, osteoarthritis, and cachexia, which are common in old age.

Finally, senescence is critical in the etiology of various diseases, such as cardiovascular diseases and osteoarthritis, during old age. However, preventing or disrupting senescence can help delay the health decline as individuals age. Targeting senescence using techniques such as senolytics and SASP-modulating drugs can help disrupt senescence and enhance the general health span of individuals as they age. Accordingly, success in using these strategies can help improve the quality of life of older adults.