{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWNT10B is a pivotal ligand of the canonical Wnt/β‐catenin pathway that plays an essential role in skeletal remodeling and osteogenesis. It is expressed by osteoclasts to help recruit and stimulate the differentiation of mesenchymal progenitors into osteoblasts, thereby coupling bone resorption with new bone formation. Dysregulation of WNT10B activity has also been linked to osteosarcoma, where aberrant signaling converges on NF‐κB and Notch pathways, and genetic studies have identified variants that correlate with altered bone mineral density and cortical bone geometry. These findings underscore WNT10B’s fundamental role in maintaining skeletal homeostasis and quality."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn various malignancies, WNT10B emerges as a critical driver of tumor progression and chemoresistance. In triple‐negative breast cancer, its overexpression leads to the activation of transcriptionally active β‐catenin and upregulation of developmental regulators such as HMGA2, thereby promoting aggressive proliferation. Similarly, in endometrial cancer, elevated levels of WNT10B enhance cell migration and proliferation—effects that are modulated by regulatory microRNAs. Deregulated WNT10B signaling has also been implicated in prostate and skin cancers, while epigenetic alterations, including promoter methylation, further affect its expression in hepatocellular and colon cancers. Together, these studies position WNT10B as a promising therapeutic target in oncology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nWNT10B also plays a significant role in metabolic regulation by modulating adipogenesis. In cellular and animal models, it acts as a negative regulator of adipocyte differentiation, an effect influenced by environmental factors such as hypoxia and endocrine disruptors (including certain pyrethroid insecticides and estrogen). Genetic association studies further link functional variants in WNT10B with differences in fat accumulation and abdominal adipose tissue distribution, while its angiogenic properties in adipose tissue suggest a multifaceted role in energy homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDuring embryonic development, proper WNT10B signaling is crucial for limb and tooth formation. Mutations and sequence variants in WNT10B have been linked to congenital anomalies such as split‐hand/foot malformation (SHFM) and various forms of dental agenesis (including oligodontia), as demonstrated by studies in diverse populations. These findings illustrate that loss‐of‐function or hypomorphic alleles of WNT10B can disrupt normal tissue patterning, leading to a spectrum of developmental malformations."}, {"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": "\nIn addition to its roles in development and metabolism, WNT10B contributes to tissue repair and regenerative processes. It modulates the fibroblast-to-myofibroblast transition during wound healing, facilitates periodontal regeneration via crosstalk with T cells, and promotes proliferation of corneal endothelial cells through dual β‐catenin-dependent and -independent mechanisms. Moreover, increased expression of WNT10B after myocardial infarction suggests that it may be involved in cardiac repair, and its regulation in psoriatic skin following UVB exposure further attests to its role in inflammatory and regenerative responses. Recent observations in trophoblast cells also hint at a potential involvement in placental differentiation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Larry Pederson, Ming Ruan, Jennifer J Westendorf, et al. 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