microRNAs as a New Mechanism Regulating Adipose Tissue Inflammation in Obesity and as a Novel Therapeutic Strategy in the Metabolic Syndrome

Figure 1

Scheme for the miRNA-mediated mechanisms in regulating white adipose tissue inflammation. The miR-132 activates NF-κB and the transcription of downstream adipokines IL-8 and MCP-1. The miR-223 played a crucial role in modulating macrophage polarization, which suppresses the infiltration of proinflammatory M1 “classically activated” macrophages by targeting Pknox1. The miR883b-5p, which is upregulated by ApN represses the expression and secretion of LBP, a LPS facilitator. The miR-126 reduces the production of CCL2 by targeting directly the 3′-UTR of CCL2, while miR-193b inhibited indirectly the CCL2 production through downregulating the transcription factors of CCL2 (RELB, STAT6, and ETS1). The microvesicles released by adipocytes may either go into circulation or transfer into the neighboring adipocytes or macrophages, probably acting as inflammatory communicators between adipocytes, macrophages, and distant cells. The arrows indicate stimulation or activation; blunted arrows indicate inhibition. ApN, adiponectin; LBP, LPS-binding protein; LPS, lipopolysaccharide; CCL2, chemokine (C-C motif) ligand 2, adapted from [5].