{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐181a is emerging as a critical regulator of immune function and cellular differentiation. In T lymphocytes from elderly individuals, diminished miR‐181a levels lead to increased expression of the phosphatase DUSP6 and impaired T cell receptor–induced ERK signaling, effects that can be reversed by restoring miR‐181a expression. In parallel, miR‐181a enhances natural killer cell differentiation by repressing inhibitors of Notch signalling, and its dysregulation in B and T cells is associated with altered immune tolerance and chronic autoimmune conditions. These findings underscore a pivotal role for miR‐181a in fine‐tuning immune cell activation, differentiation, and senescence."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in lymphocyte programming, miR‐181a modulates key regulators of endocrine and inflammatory responses. For instance, in renal medullary cells, miR‐181a controls the expression of renin and related genes, thereby contributing to mechanisms underlying essential hypertension. In oral fibroblasts from dental pulps, miR‐181a directly binds to the 3′UTR of interleukin‐8 mRNA, modulating pro‐inflammatory signals that are central to tissue homeostasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer, miR‐181a has context‐dependent and multifaceted roles that often tip the balance toward tumor progression, chemoresistance, and metastasis. In hematological malignancies such as myeloid leukemia and chronic lymphocytic leukemia, miR‐181a modulates cell cycle regulators and pro‐apoptotic proteins (e.g. p27^Kip1 and BCL‐2), influencing differentiation and resistance to agents like daunorubicin and cytarabine. In various solid tumors—including gastric, colorectal, ovarian, cervical, breast, osteosarcoma, and hepatocellular carcinoma—miR‐181a functions as an oncogenic microRNA by targeting critical tumor suppressors such as KLF6, PTEN, Smad7, and NDRG2; in addition, it down‐regulates mediators of apoptosis (e.g. Bim, PRKCD and BAX) and modulates angiogenic (via SRCIN1) and metabolic pathways (via the AKT cascade). Together, these studies demonstrate that miR‐181a deregulation contributes to enhanced cell survival, epithelial–mesenchymal transition, invasive behavior, and drug resistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "31"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies have highlighted the diagnostic and regulatory dimensions of miR‐181a in non‐cancer settings. Circulating miR‐181a levels are elevated in patients with mild cognitive impairment who later convert to Alzheimer’s disease, correlating with biomarkers of amyloid pathology and hippocampal atrophy. Exosomal miR‐181a–5p, induced by flow‐responsive transcription factors, acts cooperatively with other miRNAs to inhibit pulmonary vascular remodeling in pulmonary arterial hypertension. Moreover, in disorders of the spine such as ossification of the posterior longitudinal ligament, miR‐181a–5p facilitates osteogenic differentiation by directly targeting transcriptional regulators and modulating chromatin marks."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "32", "end_ref": "34"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, miR‐181 family members also contribute to stem cell pluripotency and metabolic regulation. 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