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Vessel Plus 2022;6:[Accepted].10.20517/2574-1209.2022.26© The Author(s) 2022
Accepted Manuscript
Open AccessReview

The complex role of RhoA in regulating vascular smooth muscle cell phenotype in type 2 diabetes

Correspondence Address: Dr. Kirsten Riches-Suman, Cardiovascular Research Group, School of Chemistry and Biosciences, Richmond Road, University of Bradford, Bradford BD7 1DP, United Kingdom. E-mail: k.riches@bradford.ac.uk

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© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Abstract

The incidence of type 2 diabetes mellitus (T2DM) is growing globally and the major cause of morbidity and mortality in these patients is the premature development of cardiovascular disease. Consequently, medical interventions including coronary artery bypass graft surgery and widespread statin prescriptions are common in this patient group. Smooth muscle cells are the major structural component of the vascular wall. They play a crucial role in post-bypass recovery to successfully revascularize the heart by switching between differentiated (contractile) and dedifferentiated (synthetic) phenotypes. However, in T2DM patients, these cells have functional defects that may affect bypass integration. RhoA is a small GTPase that regulates many functions including motility and phenotypic regulation of smooth muscle cells. Dependent upon stimulus, RhoA can drive both the contractile SMC phenotype seen in health, or mal/adaptive phenotypes prevalent in disease or in response to injury. We hypothesize that RhoA deregulation may play a significant role in the vascular complications of T2DM. This protein is deregulated in T2DM smooth muscle cells which may in part explain the functional defects of smooth muscle tissue and subsequent failure rates for bypass in these patients. An important consideration in this circumstance is the use of statin therapies as these further inhibit RhoA activity. The impact of this for T2DM bypass patients is currently unknown.

Cite This Article

Asare-Amankwah Y, Riches-Suman K. The complex role of RhoA in regulating vascular smooth muscle cell phenotype in type 2 diabetes. Vessel Plus 2022;2:[Accept]. http://dx.doi.org/10.20517/2574-1209.2022.26

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