Recent advances on the association of apoptosis in chronic non healing diabetic wound

Abstract

Generally, wounds are of two categories, such as chronic and acute. Chronic wounds takes time to heal when compared to the acute wounds. Chronic wounds include vasculitis, non healing ulcer, pyoderma gangrenosum, and diseases that cause ischemia. Chronic wounds are rapidly increasing among the elderly population with dysfunctional valves in their lower extremity deep veins, ulcer, neuropathic foot and pressure ulcers. The process of the healing of wounds has several steps with the involvement of immune cells and several other cell types. There are many evidences supporting the hypothesis that apoptosis of immune cells is involved in the wound healing process by ending inflammatory condition. It is also involved in the resolution of various phases of tissue repair. During final steps of wound healing most of the endothelial cells, macrophages and myofibroblasts undergo apoptosis or exit from the wound, leaving a mass that contains few cells and consists mostly of collagen and other extracellular matrix proteins to provide strength to the healing tissue. This review discusses the various phases of wound healing both in the chronic and acute wounds especially during diabetes mellitus and thus support the hypothesis that the oxidative stress, apoptosis, connexins and other molecules involved in the regulation of chronic wound healing in diabetes mellitus and gives proper understanding of the mechanisms controlling apoptosis and tissue repair during diabetes and may eventually develop therapeutic modalities to fasten the healing process in diabetic patients.

Keywords: Apoptosis; Diabetes mellitus; Diabetic foot; Chronic wound; Oxidative stress

Core tip: Uncontrolled diabetes mellitus lead to the chronic non healing wound which further can escort to the Ischemia and coronary artery disease. Reports suggested that the involvement of various mechanisms in the development of chronic non healing wound in patients with diabetes mellitus, among which the oxidative stress plays a pivotal role which then leading to the enhanced apoptosis of lymphocytes, may be playing a critical role in the delay of wound healing. Connexins are gap junction protein and their upregulation during diabetes might be leads to improper gap junction formation attributing to the passage of various, apoptotic and inflammatory signals thereby resulting in delayed healing of chronic diabetic ulcers.