Fight Aging!

A growing body of evidence points to a significant role for senescent cells in the aging of skin, including the work of some researchers who believe that changes that occur in skin over early adult life may be influenced by the presence of senescent cells. Skin is a large organ and its state of inflammation does influence the rest of the body. It remains to be seen as to whether presently available senolytic therapies can produce a meaningful effect on the burden of senescent cells in skin, and to what degree that will affect manifestations of skin aging in humans.

Skin 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.

Link: https://doi.org/10.1111/acel.14054