Abstract
Aging and cellular senescence are known contributors to the pathophysiology of diabetic nonhealing wounds. However, the dynamic interplay of senescent cells in diabetic wounds is not well understood. Wilkinson et al. show that macrophages, which constitute a large portion of accumulated senescent cells, release a senescence-associated secretory profile (SASP) that is rich in CXCR2 ligands, which drive fibroblasts toward a profibrotic and senescent phenotype. A selective CXCR2 antagonist promoted healing of diabetic wounds, showing a new avenue for potential therapeutic developments.
