Abstract
Background. Aging represents a complex biological process characterized by the progressive accumulation of molecular and cellular alterations that ultimately lead to a decline in tissue functional capacity and the development of age-associated diseases. The concept of the hallmarks of aging provides a systematic framework for analyzing the mechanisms underlying biological aging. In recent years, accumulating evidence has highlighted the important role of the small GTPase Cdc42 in the regulation of aging-related processes at multiple levels of cellular organization. This review presents an analysis of current studies addressing the impact of Cdc42 on all three categories of aging hallmarks—primary, antagonistic, and integrative. The mechanisms through which Cdc42 contributes to genomic instability, epigenetic alterations, cellular senescence, oxidative stress, and impaired intercellular communication, including SASP-dependent processes, are discussed. Particular attention is given to the role of Cdc42 in the regulation of cytoskeletal dynamics, mitochondrial function, and the DNA damage response. The potential of pharmacological inhibition of Cdc42 is also considered as a promising approach for correcting age-associated cellular dysfunctions and developing geroprotective strategies. This review underscores the central role of Cdc42 in the biology of aging and provides a foundation for future studies aimed at slowing age-related physiological processes and promoting functional longevity. Keywords: Cdc42, aging, cellular senescence, hallmarks of aging, mesenchymal stem cells, genomic instability, oxidative stress, SASP, epigenetic alterations, geroprotection.