A New Insight into the Roles of MiRNAs in Metabolic Syndrome

Yuxiang Huang, Yuxiang Yan, Weicheng Xv, Ge Qian, Chijian Li, Hequn Zou, Yongqiang Li, Yuxiang Huang, Yuxiang Yan, Weicheng Xv, Ge Qian, Chijian Li, Hequn Zou, Yongqiang Li

Abstract

Metabolic syndrome (MetS), which includes several clinical components such as abdominal obesity, insulin resistance (IR), dyslipidemia, microalbuminuria, hypertension, proinflammatory state, and oxidative stress (OS), has become a global epidemic health issue contributing to a high risk of type 2 diabetes mellitus (T2DM). In recent years, microRNAs (miRNAs), used as noninvasive biomarkers for diagnosis and therapy, have aroused global interest in complex processes in health and diseases, including MetS and its components. MiRNAs can exist stably in serum, liver, skeletal muscle (SM), heart muscle, adipose tissue (AT), and βcells, because of their ability to escape the digestion of RNase. Here we first present an overall review on recent findings of the relationship between miRNAs and several main components of MetS, such as IR, obesity, diabetes, lipid metabolism, hypertension, hyperuricemia, and stress, to illustrate the targeting proteins or relevant pathways that are involved in the progress of MetS and also help us find promising novel diagnostic and therapeutic strategies.

Figures

Figure 1
Figure 1
The red arrowhead represents inhibition. ① miR-499-5p, miR-181a-5p, and miR-23a-3p: the overexpression of miR-499-5p can directly downregulate PTEN, which can inhibit the PI3K/AKt pathway. As a result, they can improve the IR. ② miR-143: the overexpression of miR-143 can inhibit the insulin-induced Akt activation to cause an IR. ③ miR-145: miR-145 can inhibit the phosphorylation of IRS-1 and Akt. ④ miR-190b: miR-190b can decrease the level of IGF-1. ⑤ miR-21: miR-21 can inhibit the TGF-β1/Smad3 pathway. ⑥ miR-222 and miR-93, miR-106b: inhibit the GLUT4. ⑦ miR-30d: inhibits PI3K.

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Source: PubMed

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