MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy
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rdiovascular Diabetology Open Access
REVIEW
MicroRNAs and obesity‑induced endothelial dysfunction: key paradigms in molecular therapy Karima Ait‑Aissa1* , Quynh My Nguyen2, Mohanad Gabani1, Adam Kassan3, Santosh Kumar1, Soo‑Kyoung Choi4, Alexis A. Gonzalez5, Tahsin Khataei1, Amal M. Sahyoun6, Cheng Chen7 and Modar Kassan1*
Abstract The endothelium plays a pivotal role in maintaining vascular health. Obesity is a global epidemic that has seen dramatic increases in both adult and pediatric populations. Obesity perturbs the integrity of normal endothelium, leading to endothelial dysfunction which predisposes the patient to cardiovascular diseases. MicroRNAs (miRNAs) are short, single-stranded, non-coding RNA molecules that play important roles in a variety of cellular processes such as differentiation, proliferation, apoptosis, and stress response; their alteration contributes to the development of many pathologies including obesity. Mediators of obesity-induced endothelial dysfunction include altered endothelial nitric oxide synthase (eNOS), Sirtuin 1 (SIRT1), oxidative stress, autophagy machinery and endoplasmic reticulum (ER) stress. All of these factors have been shown to be either directly or indirectly caused by gene regulatory mechanisms of miRNAs. In this review, we aim to provide a comprehensive description of the therapeutic potential of miRNAs to treat obesity-induced endothelial dysfunction. This may lead to the identification of new targets for interventions that may prevent or delay the development of obesity-related cardiovascular disease. Keywords: MicroRNAs, Obesity, Endothelial dysfunction, Cardiovascular diseases Background Obesity is a major worldwide public health issue [1]. In the past decade, the incidence of obesity has rapidly risen to epidemic proportions [2, 3]. In the United States, obesity continues to be one of the leading public health crises. Almost a third of the American population is affected by obesity (Body mass index (BMI) > 30), and 60% fall into the overweight category (BMI > 25) [4, 5]. It is crucial to address and treat obesity because it is classified as a risk factor in the development of cardiovascular disease [6]. Diverse mechanisms by which obesity promotes cardiovascular disease have been proposed, *Correspondence: karima‑ait‑[email protected]; modar‑[email protected] 1 Cardiovascular Division, Department of Medicine, and Abboud Cardiovascular Research Center, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA Full list of author information is available at the end of the article
and most involve endothelial dysfunction [7]. Vascular function assessments in subjects with obesity have demonstrated altered properties of endothelial function [8, 9]. Many studies have established that endothelial dysfunction can be considered as the first step in the progression of cardiovascular disease [10–13]. Thus, a better understanding of the mediators of obesity-induced endothelial dysfunction will help us to identify new targets for interventions that may preve
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