Ask about this productRelated genes to: OSMR Blocking Peptide
- Gene:
- OSMR NIH gene
- Name:
- oncostatin M receptor
- Previous symbol:
- -
- Synonyms:
- OSMRB
- Chromosome:
- 5p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-17
- Date modifiied:
- 2018-07-11
Related products to: OSMR Blocking Peptide
Related articles to: OSMR Blocking Peptide
- Primary localized cutaneous amyloidosis (PLCA) is a chronic pruritic dermatological disorder characterized by amyloid deposits in the papillary dermis, significantly impairing patients' quality of life. Although the pathogenesis of PLCA is multifaceted, emerging evidence highlights the pivotal role of dysregulated cytokines, particularly the members of interleukin-6 (IL-6) cytokines family in PLCA. Oncostatin M (OSM) mediates keratinocyte proliferation through the STAT5-KLF7 axis upon OSMRβ engagement. Pathogenic variants in OSMR disrupt receptor dimerization, thereby suppressing signal transduction. These alterations together with cytokine dysregulation concomitantly elevate the expression of AHNAK and suppress that of Bcl-xL, which accelerate keratinocyte differentiation and apoptosis respectively, leading to the thickening of the stratum corneum and amyloid fibril deposition. Furthermore, dysregulated expression of chemokine monocyte chemoattractant protein-1 (MCP-1) by pathogenic variant in IL-31RA reduces monocyte-mediated clearance of amyloid fibrils, thereby promoting their pathological retention. The mechanisms of IL-31-mediated pruritus remain to be elucidated, given the conflicting observations that while some studies report wider cutaneous innervation in FPLCA patients, others demonstrate opposing results in general lichen amyloidosis patients. This review aims to synthesize recent advances in understanding PLCA pathogenesis with a focus on IL-31 and OSM cytokines network dysregulation especially driven by pathogenic variants, and provide critical insights for identifying therapeutic targets and put forward challenges in the future. - Source: PubMed
Publication date: 2026/04/24
Teng YiZhou XingliXiao YueLei KaixinDai LunzhiLi Wei - - Source: PubMed
Publication date: 2026/04/21
Fischer Michael J MReeh Peter W - Blood-brain barrier (BBB) disruption is a major contributor to brain injury following ischemic stroke. However, current endothelial-targeted strategies for BBB protection have shown limited clinical efficacy. Glial cells are essential for maintaining BBB integrity, but the mechanisms underlying glial-mediated BBB dysfunction after ischemic stroke remain poorly defined. Here, we identify microglial oncostatin M (OSM) and astrocytic OSM receptor (OSMR) as critical mediators of BBB disruption following cerebral ischemia-reperfusion. Single-cell RNA sequencing and immunofluorescence analysis revealed selective upregulation of OSMR in astrocytes after transient middle cerebral artery occlusion and reperfusion (MCAO/R) in mice. Astrocyte-specific OSMR knockdown maintained BBB integrity by restoring aquaporin-4 polarity and tight junction protein expression in electron microscopy and dextran leakage assays, thereby reducing infarct volume and improving neurological function. To elucidate the underlying mechanism, cell-cell communication analysis and proximity ligation assays demonstrated a direct and enhanced interaction between microglial OSM and astrocytic OSMR after MCAO/R. Similarly, OSM was markedly upregulated in microglia, and microglia-specific OSM knockout reproduced the protective effects of astrocytic OSMR knockdown, thereby restoring BBB integrity. Collectively, these results support the OSM-OSMR axis as a potential therapeutic target for the preservation of BBB integrity in ischemic stroke. - Source: PubMed
Publication date: 2026/04/10
Li LianxinLi XiangLiu YangyangLi HangDing HaojieLu JinxinCao ChangYuan JinlongChen GangLi Haiying - Oncostatin M (OSM) and its receptor (OSMR) are implicated in chronic inflammatory diseases. The role of OSM in Graves' orbitopathy (GO) pathogenesis remains unclear. Here, we investigated the role of OSM-OSMR signaling in GO pathogenesis and assessed its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/04/06
Park Jeong WooChoi Soo HyunSurl DongheonKo JaesangYoon Jin Sook - Chronic pancreatitis (CP), characterized by irreversible fibrosis, is a high-risk factor for pancreatic cancer. Current therapeutic strategies remain inadequate. This study identified a significant increase in CD11c cells within fibrotic regions of CP patient pancreatic tissues, accompanied by markedly reduced expression of liver kinase B1 (Lkb1) in these cells. Animal experiments confirmed that Lkb1 deletion in CD11c cells markedly exacerbated pancreatic fibrosis. Further investigation revealed that Lkb1 deletion in CD11c cells drove the differentiation of monocytes into CD11cCD206 mixed-phenotype macrophages, leading to their accumulation in fibrotic lesions. The CCL2/CCR2 signaling axis was identified as the key pathway mediating the infiltration of these macrophages. Mechanistically, Lkb1 deletion enhanced STAT3 phosphorylation in CD11cCD206 macrophages, promoted CCL2 secretion, and thereby promoted more CD11cCD206 macrophages to infiltrate. CD11cCD206 macrophages activated pancreatic stellate cells (PSCs) via OSM binding to its receptor OSMR, thereby stimulating CCL2 production of PSCs. This recruits additional monocyte-derived macrophages to sustain PSC activation and exacerbates extracellular matrix (ECM) deposition. Concurrently, neutralization of OSM suppressed CCL2 secretion from PSCs and markedly attenuated pancreatic fibrosis. This study reveals that Lkb1 deletion in CD11c cells exacerbates CP-associated fibrosis via the OSM and CCL2/CCR2 axis, thereby presenting a potential therapeutic strategy for CP fibrosis. - Source: PubMed
Publication date: 2026/03/30
Zhang WenqingGuo ShanZhang YuRen HeLei KeZhao ChenyangYu QianLuo HongqingXiao YujingFeng XiaomingLi Xiaoyu