Journal
EXPERIMENTAL DERMATOLOGY
Volume 30, Issue 1, Pages 68-73Publisher
WILEY
DOI: 10.1111/exd.14082
Keywords
advanced glycation end products; gerontology; injury; senolytics; tissue repair
Categories
Funding
- Medical Research Council [MR/M016307/1]
Ask authors/readers for more resources
Diabetes and aging are two significant factors contributing to pathological skin healing. Recent studies suggest a potential mechanistic link between these factors. Cellular senescence appears to play a role in both diabetes, wound repair, and aging, though its exact impact remains controversial.
Arguably, the two most important causes of pathological healing in the skin are diabetes and ageing. While these factors have historically been considered independent modifiers of the healing process, recent studies suggest that they may be mechanistically linked. The primary contributor to diabetic pathology is hyperglycaemia, which accelerates the production of advanced glycation end products, a characteristic of ageing tissue. Indeed, advanced age also leads to mild hyperglycaemia. Here, we discuss emerging literature that reveals a hitherto unappreciated link between cellular senescence, diabetes and wound repair. Senescent cells cause widespread destruction of normal tissue architecture in ageing and have been shown to be increased in chronic wounds. However, the role of senescence remains controversial, with several studies reporting beneficial effects for transiently induced senescence in wound healing. We recently highlighted a direct role for senescence in diabetic healing pathology, mediated by the senescence receptor, CXCR2. These findings suggest that targeting local tissue senescence may provide a therapeutic strategy applicable to a broad range of chronic wound types.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available