Cellular senescence and aging: molecular mechanisms and convergent pathways.
TL;DR
A deeper understanding of these processes may contribute to the identification of innovative interventions for age-related disorders, such as therapies targeting specific components of the senescence-associated secretory phenotype or selectively modulating senescent cell burden.
Abstract
The frequent conceptual overlap between aging and cellular senescence has generated ambiguities in experimental approaches, biomarker usage, and therapeutic strategy development within aging research. Cellular senescence and aging are biologically distinct but interconnected processes, frequently misunderstood or used interchangeably within biomedical research and theoretical discussions. Thus, aging refers to the progressive decline in physiological integrity and function at the organismal level, while cellular senescence is a stable cell-cycle arrest triggered by various forms of stress, including DNA damage, telomere shortening, epigenetic dysregulation, and mitochondrial dysfunction. This review dissects the molecular underpinnings of both phenomena, highlighting their key differences, mechanistic overlaps, and roles in health and disease, with particular emphasis on how the accumulation of senescent cells actively contributes to age-related functional decline. In particular, we discuss emerging biomarkers and therapeutic strategies, such as senolytics and partial reprogramming. Furthermore, a deeper understanding of these processes may contribute to the identification of innovative interventions for age-related disorders, such as therapies targeting specific components of the senescence-associated secretory phenotype or selectively modulating senescent cell burden.