{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe miR‐29 family—particularly miR‐29b (including the MIR29B2 variant)—has emerged as a multifaceted regulator in cancer. In hematologic malignancies such as chronic lymphocytic leukemia, multiple myeloma and acute myeloid leukemia, miR‐29b is frequently silenced via epigenetic mechanisms (for example, by overexpressed histone deacetylases or promoter hypermethylation), which in turn facilitates the upregulation of oncogenic and anti‐apoptotic factors like Mcl‐1 and Sp1. In solid tumors, including colorectal, osteosarcoma, triple‐negative breast and gastric cancers, decreased levels of miR‐29b relieve repression on key targets such as vascular endothelial growth factor, IGF1 and STAT3, thereby promoting cell proliferation, invasion and chemoresistance. In parallel, miR‐29b has been implicated in modulating immune cell function and metabolic pathways within the tumor microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its cancer‐related functions, miR‐29b plays a pivotal role in regulating tissue remodeling and fibrogenesis. In liver and intestinal fibrotic models, enhanced miR‐29b expression counteracts TGF‐β/Smad signaling to reduce collagen synthesis and extracellular matrix deposition. Furthermore, miR‐29b promotes autophagy in retinal pigment epithelial cells, regulates osteogenic differentiation via targeting BMP1, and inhibits mesothelial–mesenchymal transition processes that contribute to peritoneal metastasis and fibrotic conditions such as Peyronie’s disease and uterine leiomyoma. Changes in circulating miR‐29b levels have also been correlated with pathological states including hypertensive nephropathy, gestational diabetes and exercise‐induced skeletal muscle remodeling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the mechanistic level, miR‐29b is subject to intricate transcriptional and epigenetic regulation that varies between cellular contexts. Comparative analyses in human and mouse models reveal that miR‐29b modulates key signaling cascades—including cell cycle control, Wnt and PI3K/Akt pathways—while specific regulatory proteins such as Vav1, C/EBPα and STAT3 further influence its transcriptional output in hormone‐responsive tissues and tumors like uterine leiomyoma."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Deepa Sampath, Chaomei Liu, Karthik Vasan, et al. 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