Disrupted calcium homeostasis: a hidden driver of cellular aging

Abstract

Calcium is a critical second messenger in cellular signaling and has increasingly been recognized as an important regulator of aging. Calcium fluxes influence electrochemical gradients across cellular membranes, ligand binding, enzyme activity, and other processes associated with age-related cellular changes. In particular, calcium plays a pivotal role in driving cells toward senescent phenotypes, including cell cycle arrest and the development of the senescence-associated secretory phenotype (SASP). Modulation of calcium signaling has therefore emerged as a potential molecular strategy to regulate the burden of senescent cells. A deeper understanding of how calcium channels, mitochondrial calcium handling, and intracellular calcium dynamics contribute to senescence may reveal new opportunities for therapeutic interventions targeting age-related diseases.

Keywords: calcium, cell, senescence, aging