ArticleNature communications2015
CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Polycystic ovary syndrome and recurrent pregnancy loss, a review of literature.Frontiers in endocrinology · 2023Pooled it
- A Bidirectional C1q/TNF-Related Protein Signature Is Associated with Disease Activity in Behçet's Disease: A Cross-Sectional Study.Diagnostics (Basel, Switzerland) · 2026Article
- Maternal Gestational Diabetes Mellitus Modulates Adipose Tissue Remodeling and CTRP6 Expression in a Depot- and Sex-Specific Manner in Mouse Offspring.Biomedicines · 2026Article
- Partial embryo loss caused by disruption of the placental hormone CTRP6 coincides with dNK cell abnormalities during pregnancy.iScience · 2026Article
- Mixed effects of complement in a chronic murine model of inflammatory erosive arthritis and pulmonary vascular disease.PloS one · 2026Article
- The C1QTNF6-MX2 Antiviral Axis Inhibits Porcine Circovirus Type 2 Replication in Porcine Macrophages.Veterinary sciences · 2025Article
- CTRP6 as a negative regulator of anti-inflammatory M2 macrophage polarization.Immunometabolism (Cobham, Surrey) · 2025Article
- Role of CTRP14/C1QL1 in motor coordination and learning across the lifespan.Physiology & behavior · 2025Article
- Comprehensive characterization of pathogenic missense CTRP6 variants and their association with cancer.BMC cancer · 2025Article
- Exploring CTRP6: a biomarker and therapeutic target in metabolic diseases.American journal of physiology. Endocrinology and metabolism · 2025Review
- Modulating the gut-immune axis to alleviate rheumatoid arthritis: mechanistic insights and therapeutic potential of traditional Chinese medicine.Frontiers in immunology · 2025Review
- Association of C1QTNF6 gene polymorphism with risk and clinical features of type 1 diabetes in Chinese: implications for ZnT8A and beta-cell function.Frontiers in immunology · 2025Article
- Complement C3 deficient mice show more severe imiquimod-induced psoriasiform dermatitis than wild-type mice regardless of the commensal microbiota.Experimental animals · 2024Article
- Circulating levels of C1q/TNF-α-related protein 6 (CTRP6) in coronary artery disease and its correlation with inflammatory markers.Journal of diabetes and metabolic disorders · 2024Article
- Characterizing the Dynamic Expression of C1q/TNF-α-Related Protein 6 (CTRP6) during Pregnancy in Humans and Mice with Gestational Diabetes Mellitus.Biomedicines · 2024Article
- The gut homeostasis-immune system axis: novel insights into rheumatoid arthritis pathogenesis and treatment.Frontiers in immunology · 2024Review
- Huangqin Qingre Chubi Capsule inhibits rheumatoid arthritis by regulating intestinal flora and improving intestinal barrier.Frontiers in pharmacology · 2024Article
- Retroelement-Age Clocks: Epigenetic Age Captured by Human Endogenous Retrovirus and LINE-1 DNA methylation states.bioRxiv : the preprint server for biology · 2023Article
- Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors.Blood advances · 2023Article
- Correlation of serum subfatin, cthrc1, ctrp3, ctrp6 levels with disease indices in patients with axial spondyloarthritis.BMC rheumatology · 2023Article
Corrections and comments
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Authors and funding
24 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is important for the host defence against infection as well as for the development of inflammatory diseases. Here we show that C1q/TNF-related protein 6 (CTRP6; gene symbol C1qtnf6) expression is elevated in mouse rheumatoid arthritis (RA) models. C1qtnf6(-/-) mice are highly susceptible to induced arthritis due to enhanced complement activation, whereas C1qtnf6-transgenic mice are refractory. The Arthus reaction and the development of experimental autoimmune encephalomyelitis are also enhanced in C1qtnf6(-/-) mice and C1qtnf6(-/-) embryos are semi-lethal. We find that CTRP6 specifically suppresses the alternative pathway of the complement system by competing with factor B for C3(H2O) binding. Furthermore, treatment of arthritis-induced mice with intra-articular injection of recombinant human CTRP6 cures the arthritis. CTRP6 is expressed in human synoviocytes, and CTRP6 levels are increased in RA patients. These results indicate that CTRP6 is an endogenous complement regulator and could be used for the treatment of complement-mediated diseases.
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