{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‑146b plays multifaceted roles in the regulation of immune and inflammatory responses. It is upregulated during adipocyte differentiation where it targets key metabolic regulators such as SIRT1 to modulate fat mobilization and obesity‐related pathways (for example."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In immune cells, miR‑146b is induced in macrophages by inflammatory signals such as LTB₄ and IL‑10, thereby controlling Toll‐like receptor signaling through downregulation of molecules like SOCS‑1 and IRF5."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " In sepsis models, upregulation of miR‑146b attenuates myocardial inflammation and apoptosis via direct repression of Notch1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", while its increased expression in T cells contributes to the regulation of germinal center responses and helps restrain excessive NF‑κB–driven immune activation, highlighting compensatory interactions within the miR‑146 family."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its immune‐regulatory roles, miR‑146b is crucial in driving cellular differentiation and tissue remodeling. It functions as a positive regulator of skeletal myoblast differentiation by directly targeting transcripts such as Smad4, Notch1, and Hmga2."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In vascular smooth muscle cells, miR‑146b is induced by PDGF‐BB and modulates phenotypic transitions that affect cell proliferation and migration"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ", while enhanced expression in pluripotent stem cells supports neural commitment via downregulation of Oct4 and interference with TGF‑β signaling."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " Moreover, miR‑146b is implicated in the pathogenesis of renal fibrosis by modulating key regulators such as BCL2, PTEN, and IFNG"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", and it contributes to perivascular adipocyte browning and to vascular remodeling in atherosclerosis through targeting proteins like Bag1 and Mmp16."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in metabolism and differentiation, miR‑146b is intimately linked to diverse disease pathogenesis and host–pathogen interactions. In infectious colitis due to Clostridium difficile, altered miR‑146b expression is associated with a shift in Th17 responses"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", while in a model of PTEN‑deficient T‑cell lymphoma, overexpression of miR‑146b delays oncogenic transformation by targeting TRAF6 and mitigating NF‑κB–mediated c‑myc induction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": " Its upregulation in macrophages also contributes to virus‐induced M2 polarization in severe fever with thrombocytopenia syndrome by targeting STAT1"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": ", and in articular chondrocytes, miR‑146b accelerates extracellular matrix degradation and apoptosis in osteoarthritis by directly targeting A2M."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": " Furthermore, during Brucella infection, increased miR‑146b impairs autophagy via Tbc1d14"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "20"}]}, {"type": "t", "text": ", and its progressive decline in macrophages with aging is linked to altered cytokine expression and mitochondrial dysfunction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "21"}]}, {"type": "t", "text": " Complementary studies on other non‑coding RNAs in lung injury and microglial activation underscore the complex regulatory networks intersecting with miR‑146b–mediated pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": " In addition, aberrant miR‑146b expression is observed in schistosomiasis and inflammatory bowel disease, where it correlates with disease severity and macrophage phenotype"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": ", and its modulation in neuronal tissues impacts neuroinflammation and behavior."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "26"}]}, {"type": "t", "text": " Finally, clinical studies point to a role for miR‑146b in reproductive disorders, as its upregulation in villous tissues from unexplained miscarriage patients impairs trophoblast function via targeting IL‑1 receptor‑associated kinase‑1 and ADAM19."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jiyun Ahn, Hyunjung Lee, Chang Hwa Jung, et al. 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