title: Alteration of endothelins: a common pathogenetic mechanism in chronic diabetic complications.
abstract: Endothelin (ET) peptides perform several physiological, vascular, and nonvascular functions and are widely distributed in a number of tissues. They are altered in several disease processes including diabetes. Alteration of ETs have been demonstrated in organs of chronic diabetic complications in both experimental and clinical studies. The majority of the effects of ET alteration in diabetes are due to altered vascular function. Furthermore, ET antagonists have been shown to prevent structural and functional changes induced by diabetes in animal models. This review discusses the contribution of ETs in the pathogenesis and the potential role of ET antagonism in the treatment of chronic diabetic complications.
authors.affiliation: Department of Pathology, The University of Western Ontario, London, Ontario, Canada. schakrab@uwo.ca
authors.forename: Subrata
authors.initials: S
authors.lastname: Chakrabarti
authors.forename: Zia Ali
authors.initials: ZA
authors.lastname: Khan
authors.forename: Mark
authors.initials: M
authors.lastname: Cukiernik
authors.forename: Gen
authors.initials: G
authors.lastname: Fukuda
authors.forename: Shali
authors.initials: S
authors.lastname: Chen
authors.forename: Suranjana
authors.initials: S
authors.lastname: Mukherjee
mesh_terms: D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000503:physiopathology; D016232:Endothelins / Q000378:metabolism*; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D010084:Oxidation-Reduction; D017466:Receptors, Endothelin / Q000378:metabolism*
chemical_list: D016232:Endothelins; D017466:Receptors, Endothelin; D009569:Nitric Oxide