Vascular Ca V 1.2 channels in diabetes.

Autor: Pereira da Silva EA; Department of Pharmacology, University of California, Davis, CA, United States., Martín-Aragón Baudel M; Department of Pharmacology, University of California, Davis, CA, United States., Hong J; Department of Pharmacology, University of California, Davis, CA, United States., Bartels P; Department of Pharmacology, University of California, Davis, CA, United States., Navedo MF; Department of Pharmacology, University of California, Davis, CA, United States., Nieves-Cintrón M; Department of Pharmacology, University of California, Davis, CA, United States. Electronic address: mcnieves@ucdavis.edu.
Jazyk: angličtina
Zdroj: Current topics in membranes [Curr Top Membr] 2022; Vol. 90, pp. 65-93. Date of Electronic Publication: 2022 Oct 03.
DOI: 10.1016/bs.ctm.2022.09.003
Abstrakt: Diabetic vasculopathy is a significant cause of morbidity and mortality in the diabetic population. Hyperglycemia, one of the central metabolic abnormalities in diabetes, has been associated with vascular dysfunction due to endothelial cell damage. However, studies also point toward vascular smooth muscle as a locus for hyperglycemia-induced vascular dysfunction. Emerging evidence implicates hyperglycemia-induced regulation of vascular L-type Ca 2+ channels Ca V 1.2 as a potential mechanism for vascular dysfunction during diabetes. This chapter summarizes our current understanding of vascular Ca V 1.2 channels and their regulation during physiological and hyperglycemia/diabetes conditions. We will emphasize the role of Ca V 1.2 in vascular smooth muscle, the effects of elevated glucose on Ca V 1.2 function, and the mechanisms underlying its dysregulation in hyperglycemia and diabetes. We conclude by examining future directions and gaps in knowledge regarding Ca V 1.2 regulation in health and during diabetes.
(Copyright © 2022 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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