title: Ca(2+) handling alterations and vascular dysfunction in diabetes.
abstract: More than 65% of patients with diabetes mellitus die from cardiovascular disease or stroke. Hyperglycemia, due to either reduced insulin secretion or reduced insulin sensitivity, is the hallmark feature of diabetes mellitus. Vascular dysfunction is a distinctive phenotype found in both types of diabetes and could be responsible for the high incidence of stroke, heart attack, and organ damage in diabetic patients. In addition to well-documented endothelial dysfunction, Ca(2+) handling alterations in vascular smooth muscle cells (VSMCs) play a key role in the development and progression of vascular complications in diabetes. VSMCs provide not only structural integrity to the vessels but also control myogenic arterial tone and systemic blood pressure through global and local Ca(2+) signaling. The Ca(2+) signalosome of VSMCs is integrated by an extensive number of Ca(2+) handling proteins (i.e. channels, pumps, exchangers) and related signal transduction components, whose function is modulated by endothelial effectors. This review summarizes recent findings concerning alterations in endothelium and VSMC Ca(2+) signaling proteins that may contribute to the vascular dysfunction found in the diabetic condition.
authors.affiliation: Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain.
authors.forename: María
authors.initials: M
authors.lastname: Fernández-Velasco
authors.affiliation: Unidad de Hipertensión, Instituto de Investigación imas12, Hospital 12 de Octubre, Madrid, Spain; Instituto Pluridisciplinar, Facultad de Farmacia, Universidad Complutense de Madrid, Spain.
authors.forename: Gema
authors.initials: G
authors.lastname: Ruiz-Hurtado
authors.affiliation: Inserm, UMR S769, Faculté de Pharmacie, Université Paris Sud, Labex LERMIT, DHU TORINO, Châtenay-Malabry, France.
authors.forename: Ana M
authors.initials: AM
authors.lastname: Gómez
authors.affiliation: Departamento de Bioquímica, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico. Electronic address: arueda@cinvestav.mx.
authors.forename: Angélica
authors.initials: A
authors.lastname: Rueda
mesh_terms: D001158:Arteries / Q000378:metabolism / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000235:genetics; D003920:Diabetes Mellitus / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology
chemical_list: D007328:Insulin; D002118:Calcium
keywords: Calcium signaling; Calcium sparks; Diabetes; Endothelium; Vascular smooth muscle cells