ArticleThe Journal of biological chemistry2009
C1q tumor necrosis factor alpha-related protein isoform 5 is increased in mitochondrial DNA-depleted myocytes and activates AMP-activated protein kinase.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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The trial behind it
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
63 citing papers in PubMed, 111 citations in OpenAlex.
- Trial
- Effects of a combined aerobic and resistance exercise program on C1q/TNF-related protein-3 (CTRP-3) and CTRP-5 levels.Diabetes care · 2013Trial
- A journey through the molecular networks of endomyocardial biopsies to explore ATTR and ALiScience · 2026Article
- The mechanism of C1q/TNF-related proteins (CTRPs) in atherosclerosis associated with type 2 diabetes mellitus.European journal of medical research · 2025Review
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- MFRP is a molecular hub that organizes the apical membrane of RPE cells by engaging in interactions with specific proteins and lipids.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The relationship between serum CTRP-5, C3a/desArg, and complement-C3 levels and hypothyroidism in women with polycystic ovary syndrome.BMC endocrine disorders · 2024Article
- How Can Promoting Skeletal Muscle Health and Exercise in Children and Adolescents Prevent Insulin Resistance and Type 2 Diabetes?Life (Basel, Switzerland) · 2024Review
- CTRP13-Mediated Effects on Endothelial Cell Function and Their Potential Role in Obesity.Cells · 2024Article
- C1QTNF5 is a novel attachment factor that facilitates the entry of influenza A virus.Virologica Sinica · 2024Article
- Highlighting the idea of exerkines in the management of cancer patients with cachexia: novel insights and a critical review.BMC cancer · 2023Review
- Serum Levels of Myonectin Are Lower in Adults with Metabolic Syndrome and Are Negatively Correlated with Android Fat Mass.International journal of molecular sciences · 2023Article
- CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.Acta pharmacologica Sinica · 2023Review
- Complement 1q/Tumor Necrosis Factor-Related Proteins (CTRPs): Structure, Receptors and Signaling.Biomedicines · 2023Review
- Circulating CTRP5 in rheumatoid arthritis: an exploratory biomarker study.BMC rheumatology · 2022Article
- C1QTNF6 promotes oral squamous cell carcinoma by enhancing proliferation and inhibiting apoptosis.Cancer cell international · 2021Article
- AMPK modulation ameliorates dominant disease phenotypes of CTRP5 variant in retinal degeneration.Communications biology · 2021Article
- ER-associated CTRP1 regulates mitochondrial fission via interaction with DRP1.Experimental & molecular medicine · 2021Article
- Cell Types Used for Cultured Meat Production and the Importance of Myokines.Foods (Basel, Switzerland) · 2021Review
- Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depletion of mtDNA in myocytes causes insulin resistance and alters nuclear gene expression that may be involved in rescuing processes against cellular stress. Here we show that the expression of C1q tumor necrosis factor alpha-related protein isoform 5 (C1QTNF5) is drastically increased following depletion of mtDNA in myocytes. C1QTNF5 is homologous to adiponectin in respect to domain structure, and its expression and secretion from myocytes correlated negatively with the cellular mtDNA content. Similar to adiponectin, C1QTNF5 induced the phosphorylation of AMP-activated protein kinase (AMPK), leading to increased cell surface recruitment of GLUT4 and increased glucose uptake. Treatment of cells with purified recombinant C1QTNF5 increased the phosphorylation of acetyl-CoA carboxylase and stimulated fatty acid oxidation. C1QTNF5-mediated phosphorylation of AMPK or acetyl-CoA carboxylase was unaffected by depletion of adiponectin receptors such as AdipoR1 or AdipoR2, which indicated that adiponectin receptors do not participate in C1QTNF5-induced activation of AMPK. Serum C1QTNF5 levels were significantly higher in obese/diabetic animals (OLETF rats, ob/ob mice, and db/db mice). These results highlight C1QTNF5 as a putative biomarker for mitochondrial dysfunction and a potent activator of AMPK.
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Registered trials
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.