{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nmiR‐29a, a key member of the miR‐29 family, has emerged as a versatile regulator of gene expression that modulates extracellular matrix and fibrosis as well as differentiation and metabolic functions. In the injured heart and diabetic kidney, miR‐29a is down‐regulated, which relieves its repression of numerous mRNAs encoding collagens, fibrillins, elastin, and other extracellular matrix components and thereby promotes cardiac fibrosis and pathological collagen deposition. In bone, miR‐29a is transcriptionally induced by canonical Wnt signaling and facilitates osteoblast differentiation by directly targeting antagonists such as Dkk1, Kremen2, and sFRP2. In pancreatic β cells and skeletal muscle, miR‐29a regulates key genes governing insulin secretion and insulin responsiveness. Moreover, reduced miR‐29a levels in epithelial and intestinal cells are linked to aberrant barrier function and tissue remodelling."}, {"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 nervous system and cancer‐related settings, miR‐29a plays an influential role in controlling disease‐relevant pathways. In Alzheimer’s disease, decreased expression of miR‐29a is associated with derepression of BACE1, a key enzyme in amyloid‐β production. Likewise, miR‐29a is predicted to target regions in the HIV–1 nef gene, implicating it in antiviral defense. In multiple malignancies—including mantle cell lymphoma, cervical and pancreatic cancers, and various solid tumors—deregulated miR‐29a expression contributes to tumorigenesis by altering cell cycle regulators (for example, CDK6), chaperones involved in collagen maturation (such as HSP47), as well as extracellular matrix proteins (e.g. LAMC1). Furthermore, miR‐29a is involved in modulating signaling pathways activated by oncogenic drivers (such as c‐Myc and Hedgehog) and in influencing chemoresistance via effects on targets like PTEN, while emerging evidence also underscores its role in angiogenic processes in glioma and in modulating metastatic potential in renal cell carcinoma."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, aberrant miR‐29a expression influences hematopoiesis and holds promise as a noninvasive biomarker in chronic diseases. In hematologic lineages, ectopic expression of miR‐29a is sufficient to confer self‐renewal properties on committed progenitors and has been implicated in the initiation of acute myeloid leukemia, while its dysregulation is evident in indolent B-cell chronic lymphocytic leukemia and during normal myeloid differentiation. In addition, altered circulating levels of miR‐29a have been associated with neurodegenerative disorders such as Parkinson’s disease and have been proposed as potential markers in other contexts including lung injury and early colorectal neoplasms. Recent studies also indicate that miR‐29a contained in tumor–derived exosomes can modulate macrophage polarization, further highlighting its role in the cross-talk between tumor cells and the immune microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Eva van Rooij, Lillian B Sutherland, Jeffrey E Thatcher, et al. 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