{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‑212 has emerged as a multifaceted regulator in various physiological and pathological contexts. In the cardiovascular system, it plays a key role in promoting pathological cardiac hypertrophy and impairing autophagy through direct targeting of anti‐hypertrophic factors (e.g. FoxO3), while its upregulation in hypertension and vascular smooth muscle cells—where factors such as circ‑Sirt1 modulate its activity to influence SIRT1 expression and NF‑κB signaling—further underscores its contribution to heart and vessel remodeling. In the brain, miR‑212 (often acting in concert with its paralogue miR‑132) is downregulated in Alzheimer’s disease and related tauopathies, with this loss leading to increased tau expression, aberrant phosphorylation (via dysregulation of effectors like GSK‑3β, PP2B and NOS1) and neuronal apoptosis, suggesting that restoring its levels may exert neuroprotective effects."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn immune cells, miR‑212 is rapidly induced upon toll‑like receptor stimulation and sustained by inflammatory cues. In monocytes, it targets critical signaling components (such as IRAK4) to attenuate pro‑inflammatory cytokine production and establish tolerance. Similarly, in natural killer cells, prolonged exposure to IL‑12 triggers the upregulation of miR‑212 (alongside miR‑132 and miR‑200a), leading to downregulation of STAT4 and consequent hyporesponsiveness. Moreover, altered expression of miR‑212 has been observed in the immune cells of patients with postpartum psychosis, suggesting a broader role in fine‑tuning immune responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, the function of miR‑212 is highly context‑dependent. In pancreatic cancer, exosome‑mediated delivery of miR‑212‑3p suppresses RFXAP, contributing to immune tolerance, whereas its overexpression in pancreatic adenocarcinoma cells (via regulation of targets such as Rb1) promotes cell cycle progression. Similarly, in gastric and colorectal tumors, decreased miR‑212 levels correlate with enhanced cell growth—potentially through derepression of targets like MeCP2—while in hepatocellular carcinoma, its ectopic expression inhibits proliferation and induces apoptosis by targeting oncogenic factors such as FOXA1. Contrasting these tumor suppressive roles, in non‑small cell lung cancer and certain prostate cancers, aberrantly high levels of miR‑212 promote proliferation, migration and invasion by downregulating tumor suppressors (for example, PTCH1 and SIRT1). In breast cancer, miR‑212 (together with miR‑132) is upregulated in doxorubicin‑resistant tumors, where it represses PTEN and activates downstream AKT/NF‑κB signaling to increase drug efflux via BCRP. In chronic lymphocytic leukemia, lower basal expression of miR‑212 is associated with disease progression, while in acute myeloid leukemia higher miR‑212 levels independently predict favorable survival outcomes. Furthermore, activation of the aryl hydrocarbon receptor can induce the miR‑212/132 cluster, mediating anti‑metastatic effects."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond these systems, miR‑212 has been implicated in other disease states. In neuropsychiatric disorders such as schizophrenia, alterations in miR‑212 levels correlate with symptom improvements during treatment. In rheumatoid arthritis, although its role remains to be fully elucidated, emerging data point to its potential involvement in modulating joint inflammation. Additionally, in temporal lobe epilepsy, increased expression of long non‑coding RNAs that sequester miR‑212 appears to promote the expression of matrix metalloproteinases, which may facilitate disease progression. Finally, in liver fibrosis, miR‑212 targeting by lncRNAs such as MEG3 contributes to the regulation of epithelial‑mesenchymal transition in hepatic stellate cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ahmet Ucar, Shashi K Gupta, Jan Fiedler, et al. 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