Molecular and Environmental Modulators of Aging: Interplay Between Inflammation, Epigenetics, and RNA Stability

Aging is a complex biological process characterized by the progressive accumulation of cellular and molecular damage, leading to functional decline and increased susceptibility to age-related diseases. Central to this process is cellular senescence, a state of irreversible cell cycle arrest that acts as both a protective mechanism against tumorigenesis and a contributor to tissue degeneration. Herein, we explore the genetic and molecular mechanisms underlying aging, with a focus on telomere dynamics, the <i>Klotho</i> gene, angiotensin-converting enzyme (ACE), and the NF-κB pathway. Telomeres, which serve as protective caps at chromosome ends, shorten with each cell division, leading to replicative senescence, while the enzyme telomerase plays a pivotal role in maintaining telomere length and cellular longevity. The <i>Klotho</i> gene encoding for an aging suppressor influences insulin/IGF-1 signaling and has antioxidant properties that protect against oxidative stress. ACE, through its dual role in regulating blood pressure and degrading amyloid-beta, impacts longevity and age-related pathologies. The NF-κB pathway drives chronic inflammation or "inflammaging," contributing to the onset of age-related diseases. Understanding these pathways offers promising avenues for therapeutic interventions to extend health span and lifespan. Targeting mechanisms such as telomerase activation, <i>Klotho</i> supplementation, ACE inhibition, and NF-κB modulation hold potential for combating the detrimental effects of aging and promoting healthier aging in the population.