Diminished and altered cellular senescence response in delayed wound healing of aging.

ABSTRACT: The transient upregulation of cellular senescence within wound tissues has been demonstrated to be an important biological process facilitating efficient tissue repair. Dysregulation of this transient wound-induced senescence-like response can result in impaired healing outcomes. Given the established age-related decline in tissue regenerative capacity, we hypothesized that alterations in this senescence response contribute to the delayed healing of cutaneous wounds in aged individuals. Our investigation demonstrated a significant delay in the closure of full-thickness dorsal skin wounds in aged mice compared to their young counterparts. Analysis of the wound microenvironment revealed a transient upregulation of senescence-associated markers (p16, p21, senescence-associated β-galactosidase

SUBMITTER: Shvedova M 

PROVIDER: S-EPMC12259030 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature