Abstract
In all living organisms, metabolic homeostasis and the immune system are the most fundamental requirements for survival. Recently, obesity has become a global public health issue, which is the cardinal risk factor for metabolic disorder. Many diseases emanating from obesity-induced metabolic dysfunction are responsible for the activated immune system, including innate and adaptive responses. Of note, inflammation is the manifest accountant signal. Deeply studied microRNAs (miRNAs) have participated in many pathways involved in metabolism and immune responses to protect cells from multiple harmful stimulants, and they play an important role in determining the progress through targeting different inflammatory pathways. Thus, immune response and metabolic regulation are highly integrated with miRNAs. Collectively, miRNAs are the new targets for therapy in immune dysfunction.
Highlights
Obesity is the result of imbalanced energy intake and expenditure, which is defined as abnormal or excessive ectopic fat accumulation in peripheral tissues that may impair health
We focus on obesity-induced metabolic disorder with the goal to illustrate the links with immune response and the role of miRNAs and to develop effective therapeutic strategies
Therapeutic Directions miRNAs are widely regarded as playing a critical role in regulating homeostasis of obesity-induced metabolic disorder and immune response by fine tuning the expression of a network of genes through posttranscriptional regulation
Summary
Obesity is the result of imbalanced energy intake and expenditure, which is defined as abnormal or excessive ectopic fat accumulation in peripheral tissues that may impair health. Obesity plays an important role in the dysfunction of the liver, cardiac, pulmonary, endocrine, and reproductive systems, resulting in serious metabolic disorders, such as diabetes, fatty liver disease, atherosclerosis, and some cancers. This imposes a spectacular burden on personal health, society, and economy. It was reported that immune cells, such as macrophages and mast cells, infiltrated adipose tissue in obese animal models [2], suggesting an immunological nature of metabolic disease This observation can clarify another study which showed that some diabetic patients treated with aspirin exhibited rapid improvement in glucose homeostasis [3]. MiR-126, miR-15a, miR-29b, miR-223, and miR-28-3p are related to T2DM, and miR-155, miR302a, and miR-712 are related to atherosclerosis [18]
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