Metformin promotes wound healing in senescent fibroblasts by regulating SIRT1 and FAP-α.
Abstract
Skin aging is associated with fibroblast senescence, impaired wound healing, and dysregulation of markers such as sirtuin 1 (SIRT1) and fibroblast activation protein-α (FAP-α). It is known that proliferation and migration decrease in aging fibroblasts, which delays the repair process. Metformin, a widely used anti-diabetic drug, can regulate cellular senescence pathways. This study evaluated the effects of metformin on wound healing and SIRT1 and FAP-α expression in senescent fibroblasts. Cellular senescence was induced in primary human dermal fibroblasts using 100 µM hydrogen peroxide (H
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
Metformin enhances wound healing in senescent fibroblasts by modulating SIRT1 and FAP-α expression. The study addresses cellular senescence, a fundamental aspect of aging, and explores a potential intervention that could improve age-related wound healing, thus contributing to longevity research.
Author of this paper? Send a correction.