RT Journal Article
T1 Metabolic syndrome inhibits store-operated Ca2+ entry and calcium-induced calcium-release mechanism in coronary artery smooth muscle.
A1 Climent Flórez, Belén
A1 Santiago E, 
A1 Sánchez Pina, Ana Alejandra
A1 Muñoz Picos, Mercedes
A1 Pérez Vizcaíno, Francisco
A1 García Sacristán, Albino
A1 Rivera De Los Arcos, Luis
A1 Prieto Ocejo, Dolores
AB Metabolic syndrome causes adverse effects on the coronary circulation including altered vascular responsiveness and the progression of coronary artery disease (CAD). However the underlying mechanisms linking obesity with CAD are intricated. Augmented vasoconstriction, mainly due to impaired Ca2+ homeostasis in coronary vascular smooth muscle (VSM), is a critical factor for CAD. Increased calcium–induced calcium release (CICR) mechanism has been associated to pathophysiological conditions presenting persistent vasoconstriction while increased store operated calcium (SOC) entry appears to activate proliferation and migration in coronary vascular smooth muscle (VSM). We analyze here whether metabolic syndrome might alter SOC entry as well as CICR mechanism in coronary arteries, contributing thus to a defective Ca2+ handling and therefore accelerating the progression of CAD.
PB Elsevier
YR 2020
FD 2020-09-17
LK https://hdl.handle.net/20.500.14352/130859
UL https://hdl.handle.net/20.500.14352/130859
LA eng
NO Climent B, Santiago E, Sánchez A, et al. Metabolic syndrome inhibits store-operated Ca2+ entry and calcium-induced calcium-release mechanism in coronary artery smooth muscle. Biochemical Pharmacology 2020;182:114222. https://doi.org/10.1016/j.bcp.2020.114222
NO Universidad Complutense de Madrid
DS Docta Complutense
RD 9 abr 2026