Diabetes is one of the most prevalent metabolic disorders and is estimated to affect 400 million of 4.4% of population worldwide in the next 20 year. In diabetes, risk to develop vascular diseases is two-to four-fold increased. Ischemic tissue injury, such as refractory wounds and critical ischemic limb (CLI) are major ischemic vascular complications in diabetic patients where oxygen supplement is insufficient due to impaired angiogenesis/neovascularization. In spite of intensive studies, the underlying mechanisms of diabetes-impaired ischemic tissue injury remain incompletely understood. Hydrogen sulfide (H2S) has been considered as a third gasotransmitter regulating angiogenesis under physiological and ischemic conditions. Here, the underlying mechanisms of insufficient H2S-impaired angiogenesis and ischemic tissue repair in diabetes are discussed. We will primarily focuses on the signaling pathways of H2S in controlling endothelial function/biology, angiogenesis and ischemic tissue repair in diabetic animal models. We summarized that H2S plays an important role in maintaining endothelial function/biology and angiogenic property in diabetes. We demonstrated that exogenous H2S may be a theraputic agent for endothelial dysfunction and impaired ischemic tissue repair in diabetes.
Keywords: Angiogenesis; Diabetes; EDHF-Mediated endothelium-dependent vascular relaxation; Hydrogen sulfide; Ischemic tissue repair.
Published by Elsevier B.V.