000			nab a22 7a 4500
999			_c15944 _d15944
003			PC15944
005			20210625062815.0
008			200526b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_92167 _aRuiz Hurtado, Gema _eInstituto de Investigación i+12
245	0	0	_aCa(2+) handling alterations and vascular dysfunction in diabetes. _h[artículo de revisión]
260			_bCell calcium, _c2014
300			_a56(5):397-407.
500			_aFormato Vancouver: Fernández-Velasco M, Ruiz-Hurtado G, Gómez AM, Rueda A. Ca(2+) handling alterations and vascular dysfunction in diabetes. Cell Calcium. 2014 Nov;56(5):397-407.
501			_aPMID: 25218935
504			_aContiene 138 referencias
520			_aMore 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.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc15944.pdf _ySolicitar documento
942			_2ddc _cREV _n0