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Abstract
Diabetic foot ulcers (DFUs) are characterized by impaired wound healing due to complex biological mechanisms.
- Cellular senescence, particularly the senescence-associated secretory phenotype (SASP), may delay healing by causing ongoing inflammation.
- Senescence affects dermal fibroblasts, macrophages, and adipose tissue cells, leading to dysfunction in these cell types.
- Molecular pathways, including p53/p21 activation and resistance to cell death, are involved in the senescence process.
- The SASP could perpetuate chronic inflammation and hinder tissue regeneration in diabetic foot ulcers.
- Therapeutic strategies targeting senescent cells, such as senolytic and senomorphic agents, are under investigation for their potential to improve healing outcomes.
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