MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy.
Karima Ait-AissaQuynh My NguyenMohanad GabaniAdam KassanSantosh KumarSoo-Kyoung ChoiAlexis A GonzalezTahsin KhataeiAmal M SahyounCheng ChenModar KassanPublished in: Cardiovascular diabetology (2020)
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.
Keyphrases
- insulin resistance
- metabolic syndrome
- weight loss
- oxidative stress
- type diabetes
- cardiovascular disease
- high fat diet induced
- weight gain
- diabetic rats
- nitric oxide synthase
- nitric oxide
- high glucose
- healthcare
- public health
- adipose tissue
- signaling pathway
- endothelial cells
- skeletal muscle
- cell death
- mesenchymal stem cells
- drug induced
- stem cells
- physical activity
- binding protein
- young adults
- single molecule
- pi k akt
- genetic diversity