{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMicroRNA‐146a is emerging as a master regulator of immune homeostasis. Initial studies demonstrated that this microRNA is critical in maintaining T regulatory cell function and in curbing excessive inflammatory responses by dampening NF‐κB activation. In this context, miR‐146a is rapidly induced following immune receptor stimulation and acts by targeting adapter proteins such as IRAK1, TRAF6, and IRAK2 to limit cytokine production during viral infection and bacterial challenge."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in T cells, miR‐146a functions broadly to restrain inflammatory signaling in diverse cell types. It modulates Toll-like receptor and RIG-I–dependent pathways through the direct repression of key signaling mediators, thereby reducing NF‐κB–dependent cytokine secretion. In addition, miR‐146a is released in exosomes from dendritic cells to be taken up by neighboring cells, enabling intercellular communication that fine-tunes immune responses. These coordinated actions help maintain an optimal balance between activation and resolution of inflammation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nExtensive investigations have further linked miR‐146a to the modulation of pathological conditions. Its regulatory influence spans from protecting the heart in peripartum cardiomyopathy and attenuating sepsis‐induced cardiac dysfunction to curbing abnormal T and B cell responses in autoimmune disease and tumor growth. In models of chronic inflammation and degenerative disorders—including diabetic wounds, neurodegenerative prion disease, and kidney injury—miR‐146a exerts a protective function by limiting the production of inflammatory mediators and fibrosis, often via suppression of key molecules such as Notch1, ErbB4, ROCK1, and components of the JAK–STAT axis. Moreover, miR‐146a impacts macrophage polarization, modulates glial cell activation in neuropathic pain, and influences stem cell differentiation in muscle and spermatogenesis, highlighting its therapeutic potential across a wide spectrum of diseases. 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