Photoaging is a distinct form of pathological skin aging driven primarily by chronic ultraviolet (UV) radiation, which clinically manifests as wrinkles, dyspigmentation, and loss of elasticity. Although core molecular events induced by UV—such as oxidative stress and DNA damage—are relatively well-understood, there is still a lack of a systematic and integrated understanding of how diverse cell types in the skin collectively drive photoaging through complex interactive networks. This review systematically elaborates the cellular and molecular mechanisms underlying skin photoaging. The key pathways involved are examined, including oxidative stress, apoptosis, dysregulated autophagy, activation of inflammatory cascades, and degradation of the extracellular matrix (ECM). This review further details the pivotal roles of and reciprocal crosstalk among fibroblasts, keratinocytes, melanocytes, and various immune cells. By providing an integrated perspective on these interactions, this review outlines the cellular and molecular mechanism of UV-associated senescence, which uniquely integrates the roles of the immune microenvironment and cellular crosstalk, providing a roadmap for next-generation anti-photoaging strategies.
Li et al. (Thu,) studied this question.