ArticleThe Journal of biological chemistry2013
Lack of oncostatin M receptor β leads to adipose tissue inflammation and insulin resistance by switching macrophage phenotype.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 71 citations in OpenAlex.
- Lipid Metabolic Dysregulation Driven by OSMR Mutations Underlies Amyloidogenesis in Primary Localized Cutaneous Amyloidosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Immunotherapy drug target identification using machine learning and patient-derived tumour explant validation.Nature machine intelligence · 2026Article
- OSMRβ-mediated signals on resident fibroblasts restore healing in diabetic skin wounds through promoting angiogenesis and granulation tissue formation.Communications biology · 2025Article
- Oncostatin-M functionalized cryogel microspheres for promoting diabetic bone defects regeneration.Journal of orthopaedic translation · 2025Article
- Novel Cell-to-Cell Communications Between Macrophages and Fibroblasts Regulate Obesity-Induced Adipose Tissue Fibrosis.Diabetes · 2025Article
- Advancements in the understanding of mechanisms of the IL-6 family in relation to metabolic-associated fatty liver disease.Frontiers in endocrinology · 2025Review
- Suppression of renal crystal formation, inflammation, and fibrosis by blocking oncostatin M receptor β signaling.Scientific reports · 2024Article
- Article
- Targeting Oncostatin M Receptor to Attenuate Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2024Article
- OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling.Journal of translational medicine · 2023Article
- Oncostatin M promotes lipolysis in white adipocytes.Adipocyte · 2022Article
- Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway.Experimental & molecular medicine · 2020Review
- Essential roles of oncostatin M receptor β signaling in renal crystal formation in mice.Scientific reports · 2020Article
- A Role for Oncostatin M in the Impairment of Glucose Homeostasis in Obesity.The Journal of clinical endocrinology and metabolism · 2020Article
- Adipocyte Oncostatin Receptor Regulates Adipose Tissue Homeostasis and Inflammation.Frontiers in immunology · 2020Review
- Tautomerase Activity-Lacking of the Macrophage Migration Inhibitory Factor Alleviates the Inflammation and Insulin Tolerance in High Fat Diet-Induced Obese Mice.Frontiers in endocrinology · 2020Article
- Oncostatin M in the Regulation of Connective Tissue Cells and Macrophages in Pulmonary Disease.Biomedicines · 2019Review
- LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway.Journal of cellular physiology · 2019Article
- EPStem cells translational medicine · 2019Article
- Review: the Roles and Mechanisms of Glycoprotein 130 Cytokines in the Regulation of Adipocyte Biological Function.Inflammation · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncostatin M (OSM), a member of the IL-6 family of cytokines, plays important roles in a variety of biological functions, including inflammatory responses. However, the roles of OSM in metabolic diseases are unknown. We herein analyzed the metabolic parameters of OSM receptor β subunit-deficient (OSMRβ(-/-)) mice under normal diet conditions. At 32 weeks of age, OSMRβ(-/-) mice exhibited mature-onset obesity, severer hepatic steatosis, and insulin resistance. Surprisingly, insulin resistance without obesity was observed in OSMRβ(-/-) mice at 16 weeks of age, suggesting that insulin resistance precedes obesity in OSMRβ(-/-) mice. Both OSM and OSMRβ were expressed strongly in the adipose tissue and little in some other metabolic organs, including the liver and skeletal muscle. In addition, OSMRβ is mainly expressed in the adipose tissue macrophages (ATMs) but not in adipocytes. In OSMRβ(-/-) mice, the ATMs were polarized to M1 phenotypes with the augmentation of adipose tissue inflammation. Treatment of OSMRβ(-/-) mice with an anti-inflammatory agent, sodium salicylate, improved insulin resistance. In addition, the stimulation of a macrophage cell line, RAW264.7, and peritoneal exudate macrophages with OSM resulted in the increased expression of M2 markers, IL-10, arginase-1, and CD206. Furthermore, treatment of C57BL/6J mice with OSM increased insulin sensitivity and polarized the phenotypes of ATMs to M2. Thus, OSM suppresses the development of insulin resistance at least in part through the polarization of the macrophage phenotypes to M2, and OSMRβ(-/-) mice provide a unique mouse model of metabolic diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.