Epac in vascular smooth muscle cells
Author | Wehbe, Nadine |
Author | Nasser, Suzanne A. |
Author | Al-Dhaheri, Yusra |
Author | Iratni, Rabah |
Author | Bitto, Alessandra |
Author | El-Yazbi, Ahmed F. |
Author | Badran, Adnan |
Author | Kobeissy, Firas |
Author | Baydoun, Elias |
Author | Eid, Ali H. |
Available date | 2023-09-25T10:26:16Z |
Publication Date | 2020 |
Publication Name | International Journal of Molecular Sciences |
Resource | Scopus |
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. |
Sponsor | represent a potential target for drugs designed to treat atherosclerosis and hypertension. It is, therefore, important that future studies identify other downstream effectors that mediate Rap1-independent EPAC signaling to facilitate the development of new therapeutics that may target this family of cAMP effectors. Extensive research is also required to resolve the discrepancies in the role of EPAC in the vasculature and to translate in vitro and in vivo studies into clinical trials. Author Contributions: N.W., S.A.N., Y.A.-D., R.I., A.B. (Alessandra Bitto), A.F.E.-Y., A.B. (Adnan Badran), F.K., E.B. and A.H.E. contributed to writing the manuscript. N.W., S.A.N. and A.H.E. led the writing of the first draft. Author Contributions: All authors contributed to writing the manuscript. N.W., S.A.N. and A.H.E. led the A.H.E. conceived, edited, and finalized the manuscript. All authors have read and agreed to the published version writing of the first draft. A.H.E. conceived, edited, and finalized the manuscript. of the manuscript. Funding: This work was supported by the American University of Beirut (Grant: MPP 320133 and Farouk Jabre Awarrdtto Allii Eiidd)),, and United Arab Emirates University (Grant #: 31S398--UPAR to Yusraa Al-Dhaheri). |
Language | en |
Publisher | MDPI |
Subject | CAMP Cardiovascular disease EPAC Phenotypic switch ROS Vascular smooth muscle cells |
Type | Article Review |
Pagination | 1-14 |
Issue Number | 14 |
Volume Number | 21 |
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