title: Insulin Resistance and Endothelial Dysfunction Constitute a Common Therapeutic Target in Cardiometabolic Disorders.
abstract: Insulin resistance and other risk factors for atherosclerosis, such as hypertension and hypercholesterolemia, promote endothelial dysfunction and lead to development of metabolic syndrome which constitutes an introduction to cardiovascular disease. The insulin resistance and endothelial dysfunction cross talk between each other by numerous metabolic pathways. Hence, targeting one of these pathologies with pleiotropic treatment exerts beneficial effect on another one. Combined and expletive treatment of hypertension, lipid disorders, and insulin resistance with nonpharmacological interventions and conventional pharmacotherapy may inhibit the transformation of metabolic disturbances to fully developed cardiovascular disease. This paper summarises the common therapeutic targets for insulin resistance, endothelial dysfunction, and vascular inflammatory reaction at molecular level and analyses the potential pleiotropic effects of drugs used currently in management of cardiovascular disease, metabolic syndrome, and diabetes.
authors.affiliation: Department of Internal Medicine, Occupational Diseases Hypertension and Clinical Oncology, Wroclaw Medical University, Ulica Borowska 213, 50-556 Wrocław, Poland; Research and Development Department, Integrated Cardiovascular Centre Provincial Specialist Hospital in Wroclaw (WROVASC), Ulica Kamieńskiego 73a, 51-124 Wrocław, Poland.
authors.forename: A
authors.identifier: 0000-0001-9806-5213
authors.initials: A
authors.lastname: Janus
authors.affiliation: Department of Internal Medicine, Occupational Diseases Hypertension and Clinical Oncology, Wroclaw Medical University, Ulica Borowska 213, 50-556 Wrocław, Poland; Research and Development Department, Integrated Cardiovascular Centre Provincial Specialist Hospital in Wroclaw (WROVASC), Ulica Kamieńskiego 73a, 51-124 Wrocław, Poland.
authors.forename: E
authors.identifier: 0000-0002-4446-6991
authors.initials: E
authors.lastname: Szahidewicz-Krupska
authors.affiliation: Department of Internal Medicine, Occupational Diseases Hypertension and Clinical Oncology, Wroclaw Medical University, Ulica Borowska 213, 50-556 Wrocław, Poland.
authors.forename: G
authors.initials: G
authors.lastname: Mazur
authors.affiliation: Department of Internal Medicine, Occupational Diseases Hypertension and Clinical Oncology, Wroclaw Medical University, Ulica Borowska 213, 50-556 Wrocław, Poland; Research and Development Department, Integrated Cardiovascular Centre Provincial Specialist Hospital in Wroclaw (WROVASC), Ulica Kamieńskiego 73a, 51-124 Wrocław, Poland.
authors.forename: A
authors.identifier: 0000-0001-5472-028X
authors.initials: A
authors.lastname: Doroszko
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000628:therapy*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000628:therapy; D007249:Inflammation; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D008055:Lipids / Q000737:chemistry; D020935:MAP Kinase Signaling System; D024821:Metabolic Syndrome / Q000378:metabolism; D018384:Oxidative Stress; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D012084:Renin-Angiotensin System; D012307:Risk Factors; D015398:Signal Transduction; D014652:Vascular Diseases / Q000503:physiopathology*
chemical_list: D007328:Insulin; D008055:Lipids; D019869:Phosphatidylinositol 3-Kinases