{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMiR‐210 is widely recognized as a master hypoxamiR induced by low oxygen tension through key transcription factors such as HIF‐1α and, in certain contexts, NF‐κB. Once induced, miR‐210 targets several critical mediators of mitochondrial metabolism—including ISCU, COX10, and GPD1L—thereby repressing iron–sulfur cluster assembly and oxidative phosphorylation while shifting energy production toward glycolysis. In addition, miR‐210 modulates placental mitochondrial function during hypoxia and contributes to metabolic adaptations in other tissues, illustrating its central role in cellular stress responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, miR‐210 exerts multifaceted functions that influence tumor progression. Cancer cells under hypoxia not only upregulate miR‐210 intracellularly but also package it into exosomes that are capable of reprogramming endothelial cells to enhance angiogenesis. Within tumor cells, miR‐210 regulates cell cycle checkpoints and modulates apoptotic responses—sometimes bypassing hypoxia‐induced cell cycle arrest via targets such as MNT or E2F3—thereby contributing to metastasis, radioresistance, and, in some cases, poor prognosis. Notably, while elevated miR‐210 levels generally support oncogenic processes in several cancers (including pancreatic, lung, head and neck, and prostate carcinomas), in certain settings such as esophageal squamous cell carcinoma its down‐regulation appears to limit cell proliferation. Furthermore, in hepatoma and other tumor types, miR‐210 has been implicated in tuning the hypoxic response within metastatic niches."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond cancer, miR‐210 plays important roles in ischemic and reparative processes. Its robust induction in hypoxic tissues, such as in ischemic wounds and infarcted myocardium, has been linked to altered cell proliferation and enhanced angiogenesis. For example, in hypoxic wound beds, miR‐210 impairs re‐epithelialization by down‐regulating cell‐cycle regulatory proteins, whereas in mesenchymal stem cell–derived exosomes miR‐210 promotes endothelial cell migration and tube formation, thereby contributing to tissue repair. Circulating levels of miR‐210 also serve as sensitive biomarkers in conditions such as cerebral ischemia, acute kidney injury, and preeclampsia—highlighting its clinical utility in diagnosing and prognosticating hypoxia‐associated pathologies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMiR‐210 also contributes to the modulation of immune and inflammatory processes as well as intercellular communication via exosomes. In autoimmune cutaneous disorders such as psoriasis, up‐regulation of miR‐210 skews T‐cell polarization toward Th17 and Th1 subsets by repressing key regulators including STAT6 and LYN, while in preeclampsia its elevated expression in trophoblasts curtails migration and invasion by targeting factors like Ephrin-A3 and HOXA9. In addition, aberrant epigenetic silencing of miR‐210 has been associated with Helicobacter pylori–driven gastric disease, and exosomal transfer of miR‐210—mediated by factors such as TIMP-1 and CTGF—further amplifies angiogenic signaling via the JAK2/STAT3 pathway and by targeting regulators such as TET2. Moreover, disturbances in miR‐210 levels can disrupt immune tolerance via modulating FOXP3 expression in regulatory T cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Xin Huang, Lianghao Ding, Kevin L Bennewith, et al. 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