Epac in vascular smooth muscle cells
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MDPI AG
Abstract
Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EPACs) have been shown to play vital roles in a plethora of pathways in different cell systems. While extensive research to identify the role of EPAC in the vasculature has been conducted, much remains to be explored to resolve the reported discordance in EPAC’s effects. In this paper, we review the role of EPAC in VSMCs, namely its regulation of the vascular tone and phenotypic switching, with the likely involvement of reactive oxygen species (ROS) in the interplay between EPAC and its targets/effectors. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
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Camp, Cardiovascular disease, Epac, Phenotypic switch, Ros, Vascular smooth muscle cells, Animals, Cell movement, Cell proliferation, Guanine nucleotide exchange factors, Humans, Mitochondria, Muscle contraction, Muscle, smooth, vascular, Myocytes, smooth muscle, Reactive oxygen species, Signal transduction, Adenosine triphosphate sensitive potassium channel, Cyclin d1, Endothelial nitric oxide synthase, G protein coupled receptor, Mammalian target of rapamycin complex 1, Mitogen activated protein kinase 3, Myosin light chain kinase, Myosin light chain phosphatase, Nitric oxide, Nuclear receptor nur77, Protein kinase b, Voltage gated calcium channel, Guanine nucleotide exchange factor, Rapgef3 protein, human, Reactive oxygen metabolite, Ampk signaling, Angiogenesis, Atherosclerosis, Blood vessel tone, Carotid artery ligation, Cell migration, Exchange protein activated by camp, Extracellular matrix, Gene, Human, Hyperpolarization, Phenotype, Protein degradation, Protein phosphorylation, Reperfusion injury, Review, Sequence homology, Smooth muscle cell, Tumor microenvironment, Vascular smooth muscle cell, Wound healing, Animal, Cell motion, Genetics, Metabolism, Mitochondrion, Pathology, Physiology, Vascular smooth muscle