Abstract
Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.
Highlights
Metabolic syndrome (MetS) constitutes a cluster of at least three out of five of the conditions including central obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL)
The most popular definition used for surveys and health care plan is by IDF (International Diabetes Federation) 2006 [3,4]: Waist > 94 cm or > 80 cm in Europe, > 102 cm or > 88cm in USA, > 90 cm or > 80 cm in Asia, along with the presence of 2 or more of the following: Blood glucose greater than 5.6 mmol/L (100 mg/dl) or diagnosed diabetes HDL cholesterol < 1.0 mmol/L (40 mg/dl) in men, < 1.3 mmol/L (50 mg/dl) in women or drug treatment for low HDL-C Blood triglycerides (TG) > 1.7 mmol/L (150 mg/dl) or drug treatment for elevated triglycerides Blood pressure > 130/85 mmHg or drug treatment for hypertension (HT)
The purpose of this review is to present the progress made in this field, describing mechanistic miRNAs-driven gene expression regulation during Oxidative stress (OxS) and MetS progression
Summary
Metabolic syndrome (MetS) constitutes a cluster of at least three out of five of the conditions including central obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL). The molecular mechanisms of obesity and other features of MetS are not yet fully elucidated, while many studies indicate the increasing involvement of epigenetics including microRNAs (miRNAs) [5] These non-coding single-stranded RNAs, approximately 19–25 nucleotides long, are involved in the transcriptional and post-transcriptional regulation of gene expression by specific interactions with target genes [6,7]. Investigation of miRNAs and their targets may potentially identify new pathways involved in the pathogenesis of metabolic diseases, improving our understanding of the molecular mechanisms influencing the relationship between miRNAs and OxS in MetS. This in turn could be useful for the development of new therapeutic approaches that enable the effective treatment of IR and impaired metabolism of white adipose tissue (WAT) under metabolic stress. The purpose of this review is to present the progress made in this field, describing mechanistic miRNAs-driven gene expression regulation during OxS and MetS progression
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