Research progress on cell cycle arrest in dermal fibroblasts.
Abstract
Cell cycle arrest in dermal fibroblasts is a critical biological process essential for maintaining skin homeostasis and serves as a central mechanism driving various skin pathologies. This review systematically summarizes the endogenous and exogenous factors triggering cell cycle arrest in dermal fibroblasts and their underlying molecular mechanisms, with a particular focus on the roles of key signaling pathways such as p53, TGF-β/Smad, and Wnt/β-catenin. Additionally, the dual effects of cell cycle arrest on the skin are discussed: transient arrest facilitates DNA damage repair and tissue regeneration, whereas prolonged arrest leads to cellular senescence, chronic inflammation, collagen degradation, and fibrosis. Advances in chemical compounds modulating cell cycle arrest are also highlighted, including potential therapeutic strategies for promoting or relieving cell cycle arrest. This review provides new insights into skin regenerative medicine and anti-aging therapies while identifying critical scientific questions for future research.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
Cell cycle arrest in dermal fibroblasts can have both regenerative and detrimental effects on skin health. The paper is relevant as it explores mechanisms that could influence aging processes and skin regeneration, which are critical in the context of longevity research.
Author of this paper? Send a correction.