{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMIAT was originally identified as a novel long noncoding transcript associated with myocardial infarction and has since emerged as a versatile regulator in the cardiovascular system. In several studies, MIAT is shown to modulate transcriptional activity and allele‐specific nuclear protein binding, contributing to myocardial infarction susceptibility, destabilization of atherosclerotic plaques through inhibition of apoptotic cell clearance, and altered gene expression in ischemic stroke. Moreover, MIAT is induced under pathological conditions such as oxidized‐LDL exposure where it mediates endothelial dysfunction and even participates in cardiomyocyte apoptosis and heart failure. These observations collectively implicate MIAT as a critical factor in cardiovascular and cerebrovascular disease pathogenesis."}, {"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 the central nervous system, MIAT (also known as Gomafu) has been implicated in neural development and the regulation of alternative splicing. Notably, dysregulation of MIAT has been linked to schizophrenia, where its abnormal expression and interaction with splicing factors contribute to aberrant splicing patterns of schizophrenia‐associated genes. Such findings underscore a potential role for MIAT as a molecular contributor to neuropsychiatric disorders."}, {"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": "\nA wealth of evidence now supports an oncogenic and/or protumorigenic function for MIAT across a broad spectrum of cancers. In endocrine and epithelial malignancies—from neuroendocrine prostate cancer and chronic lymphocytic leukemia to non‐small cell lung, breast, gastric, papillary thyroid, pancreatic, esophageal, ovarian, tongue squamous cell carcinoma, clear cell renal cell carcinoma, melanoma, osteosarcoma, and acute myeloid leukemia—MIAT is frequently overexpressed. In these settings, MIAT generally acts as a competing endogenous RNA (ceRNA) that sponges various tumor‐suppressive microRNAs (for example, miR-150‐5p, miR-29a-3p, miR-133, miR-128-3p, and others), leading to the de‐repression of oncogenic targets such as EZH2, HDAC4, ZEB1, SIRT1, VEGFC, INCENP, and cyclin D1. This intricate network of post‐transcriptional regulation not only promotes proliferation, migration, invasion, and survival of malignant cells but also mediates resistance to therapeutic agents. Collectively, these studies position MIAT as both a promising diagnostic biomarker and an attractive therapeutic target in cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in cardiovascular, neurological, and oncogenic contexts, MIAT also participates in a range of other biological processes and disease states. In mesenchymal stem cells, MIAT expression decreases during osteogenic differentiation, implicating it as a negative regulator of bone formation. In benign uterine leiomyoma, MIAT functions as a sponge for microRNAs to modulate extracellular matrix accumulation. Moreover, MIAT has been linked to fibrotic responses in chronic pancreatitis, contributed to increased corneal neovascularization by regulating endothelial permeability, and modulated macrophage autophagy and apoptosis during Mycobacterium tuberculosis infection. These diverse roles further emphasize the broad functional significance of MIAT in human pathology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "37", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nobuaki Ishii, Kouichi Ozaki, Hiroshi Sato, et al. 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