Affiliation:
1. Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education) Tianjin Medical University Tianjin China
2. Dermatology Hospital Southern Medical University Guangdong China
3. Department of Dermatology University of California San Francisco and Veterans Affairs Medical Center San Francisco California USA
Abstract
AbstractSkin aging is characterized by changes in its structural, cellular, and molecular components in both the epidermis and dermis. Dermal aging is distinguished by reduced dermal thickness, increased wrinkles, and a sagging appearance. Due to intrinsic or extrinsic factors, accumulation of excessive reactive oxygen species (ROS) triggers a series of aging events, including imbalanced extracellular matrix (ECM) homeostasis, accumulation of senescent fibroblasts, loss of cell identity, and chronic inflammation mediated by senescence‐associated secretory phenotype (SASP). These events are regulated by signaling pathways, such as nuclear factor erythroid 2‐related factor 2 (Nrf2), mechanistic target of rapamycin (mTOR), transforming growth factor beta (TGF‐β), and insulin‐like growth factor 1 (IGF‐1). Senescent fibroblasts can induce and accelerate age‐related dysfunction of other skin cells and may even cause systemic inflammation. In this review, we summarize the role of dermal fibroblasts in cutaneous aging and inflammation. Moreover, the underlying mechanisms by which dermal fibroblasts influence cutaneous aging and inflammation are also discussed.
Funder
National Natural Science Foundation of China