{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn the nervous system, miR‑132 acts as an activity‐dependent regulator that promotes dendritic growth and synaptic plasticity by repressing targets such as p250GAP, thereby facilitating proper neuronal circuit formation. Loss or dysregulation of miR‑132 has been implicated in neurodegenerative disorders including Alzheimer’s disease, where its reduced expression contributes to tau hyperphosphorylation, aggregation, and neuronal apoptosis. In addition, altered miR‑132 levels are associated with neurodevelopmental and psychiatric conditions—such as schizophrenia and major depressive disorder—where deficient miR‑132 correlates with impaired cholinergic function and cognitive decline, while its replacement can restore adult hippocampal neurogenesis and memory function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various malignancies, miR‑132 exhibits context‐dependent functions that can either suppress or promote tumorigenesis. In pancreatic and hepatocellular carcinomas, aberrant miR‑132 expression—whether by over‐expression or epigenetic silencing—modulates key pathways (including those involving Rb1 and Akt) to influence cell cycle progression and proliferation. Similarly, in cancers of the prostate, lung, breast, pituitary gland, glioma, colorectal region, and bladder, miR‑132 directly targets genes such as ZEB2, HN1, and others, or interacts with long non‐coding RNAs to regulate epithelial–mesenchymal transition, invasiveness, and metastatic potential. These findings underscore the dualistic role of miR‑132 in cancer development, with its impact depending on the cellular context and epigenetic landscape."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in neural development and cancer, miR‑132 critically modulates immune and inflammatory responses as well as vascular and wound‐healing processes. Rapid induction of miR‑132 during viral infections and Toll‐like receptor activation leads to suppression of interferon‐stimulated genes and promotion of immune tolerance via targets such as p300 and IRAK4. In metabolic tissues, miR‑132 influences the production of proinflammatory cytokines by inhibiting SirT1–mediated deacetylation of NF‑κB, thereby linking nutrient status to inflammation. Moreover, miR‑132 orchestrates angiogenic responses and keratinocyte proliferation during wound repair, and its dysregulation is associated with conditions ranging from hypertension to chronic ulceration. 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