{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe oncostatin M receptor (OSMR) is a pivotal component of cytokine‐mediated signaling that binds oncostatin M—and in certain contexts interleukin‑31—to initiate robust downstream pathways such as the JAK/STAT cascade. This receptor–ligand interaction regulates inflammatory gene expression and promotes production of proinflammatory cytokines and chemokines in diverse tissues, contributing to disease states including inflammatory bowel diseases and autoimmune disorders. Soluble forms and genetic polymorphisms of OSMR further modulate these responses and may influence therapeutic outcomes in anti‑TNF–resistant patients."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its inflammatory functions, OSMR plays an important role in tissue remodeling and repair. In the cardiovascular system, its activation participates in cardiomyocyte remodeling following injury and is rapidly upregulated after arterial damage. Similarly, OSMR‐dependent signaling has been implicated in neuroprotective mechanisms during ischemic stroke, in kidney injury, and in hepatic responses to chronic inflammation—highlighting its broad capacity to regulate organ‐specific stress responses and remodeling processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant regulation of OSMR is a common feature in numerous human cancers. In epithelial malignancies such as colorectal, ovarian, cervical, and bladder cancers, changes in OSMR expression—via epigenetic silencing, gene methylation, copy-number gains, or alternative splicing—can enhance tumor cell migration, invasion, angiogenesis, and resistance to apoptotic signals. In glioblastoma, for example, an OSMR–STAT3 axis drives a mesenchymal and highly invasive phenotype, whereas in melanoma, epigenetic repression of OSMR helps tumor cells escape growth inhibition. Moreover, interactions between IL‑31 and OSMR have been implicated in B-cell lymphoma, underscoring the receptor’s multifaceted roles in cancer progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic alterations in the OSMR gene have been linked with distinct cutaneous and neuroendocrine phenotypes. Missense mutations and pathogenic variants are associated with familial primary localized cutaneous amyloidosis, where disrupted receptor function in keratinocytes leads to aberrant epidermal differentiation and chronic pruritus. In some pedigrees, OSMR variants have also been detected alongside endocrine abnormalities such as medullary thyroid carcinoma or in association with Hirschsprung‐related enterocolitis. Structural analyses of OSMR further elucidate the critical receptor–ligand interfaces that determine its signaling specificity and downstream biological functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nathaniel R West, Ahmed N Hegazy, Benjamin M J Owens, et al. 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