Zombie Cells in the Wound: How Senescent Fibroblasts Sabotage Diabetic Ulcers

Dr. G examines how normal fibroblasts drive tissue repair and how, in diabetic foot ulcers, they can become senescent “zombie” cells that stop dividing, secrete inflammatory SASP factors, and degrade the wound environment. The episode covers triggers (hyperglycemia, oxidative stress, ischemia, infection), clinical signs and biomarkers of senescence, the vicious cycle with biofilm, and emerging approaches—including senolytics, targeted dressings, and debridement—to reduce senescent burden and improve healing.