ArticleInflammation2017
TAZ Activator Is Involved in IL-10-Mediated Muscle Responses in an Animal Model of Traumatic Brain Injury.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Hippo-YAP/TAZ signalling at the crossroads of brain ageing and neurological disorders: mechanisms, crosstalk, and therapeutic prospects.Biogerontology · 2026Review
- Obesity, Osteoarthritis, and Myokines: Balancing Weight Management Strategies, Myokine Regulation, and Muscle Health.Nutrients · 2024Review
- Emerging role and function of Hippo-YAP/TAZ signaling pathway in musculoskeletal disorders.Stem cell research & therapy · 2024Review
- Anti-Inflammatory Effect of Muscle-Derived Interleukin-6 and Its Involvement in Lipid Metabolism.International journal of molecular sciences · 2021Review
- Interleukin-6 is associated with acute concussion in military combat personnel.BMC neurology · 2020Observational
- TAZ and myostatin involved in muscle atrophy of congenital neurogenic clubfoot.World journal of clinical cases · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional coactivator with PDZ-binding motif (TAZ) functions as a downstream regulatory target in the Hippo signaling pathway that plays various roles. We previously developed a cell-based assay and identified the TAZ activator IBS008738 as a potential therapeutic target for glucocorticoid-induced atrophy. To further explore the application of IBS008738 in various muscle-related diseases, we examined the function of IBS008738 in inflammatory cytokine-mediated mouse muscle responses after traumatic brain injury (TBI). Preliminary screening suggested that IBS008738 treatments increased the levels of IL-10 in C2C12 cells. In TBI and sham control mice, we compared the effect of IBS008738 treatments on TNF α, IL-6, and IL-10 mRNA levels, muscle morphologic changes, and macrophage phenotype changes. Our findings support that the TAZ activator IBS008738 decreases muscle wasting by upregulating IL-10 and inhibiting TNF α and IL-6, and this process is implemented by changing the macrophage phenotypes. These results indicate a new mechanism of the TAZ activator as a potential therapy for atrophy.
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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.