{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nOncostatin M (OSM) is a multifunctional cytokine of the interleukin‐6 family that is produced by a variety of immune cells—including dendritic cells, neutrophils, and macrophages—and plays pivotal roles in regulating inflammation and tissue remodeling across different organ systems. In mucosal and barrier tissues, elevated OSM disrupts epithelial integrity and stimulates the production of chemokines and proinflammatory mediators, thereby contributing to chronic conditions such as inflammatory bowel disease, asthma, atherosclerosis, and even modulating cardiomyocyte dedifferentiation after myocardial injury. In addition, OSM released during bacterial challenge (for example, by dendritic cells) and in acute peritonitis further highlights its importance in initiating and timing inflammatory cell recruitment and barrier dysfunction."}, {"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": "\nIn oncogenic settings, OSM exerts profound effects on tumor cell behavior by promoting epithelial–mesenchymal transition, enhancing cancer stem cell characteristics, and driving resistance to various targeted therapies. By engaging downstream pathways such as JAK/STAT3 and PI3K, OSM contributes to an aggressive tumor phenotype in diverse cancers—including breast, prostate, non‐small cell lung, ovarian, pancreatic, and osteosarcoma—by suppressing hormone receptor expression and facilitating cellular detachment and invasion. Thus, OSM has emerged as a critical mediator of tumor plasticity and metastasis."}, {"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": "\nBeyond its roles in inflammation and oncogenesis, OSM is also a key regulator of metabolic processes, bone homeostasis, and stem cell dynamics. It modulates bone remodeling by coordinating osteoclast‐mediated resorption and osteoblast‐driven new bone formation, and influences lipid metabolism through suppression of factors such as PCSK9 in the liver. Moreover, OSM affects adipose tissue function—upregulating molecules linked to cardiovascular risk—and participates in systemic conditions such as myeloproliferative neoplasms and diabetes-associated stem cell mobilopathy. It further governs stem cell quiescence in hair follicles and signals through distinct receptor interfaces that underline its pleiotropic actions, emphasizing its diverse roles in maintaining tissue and metabolic homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "44"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Takafumi Suda, Kingo Chida, Akihito Todate, et al. 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