ArticleJournal of inflammation (London, England)2017
Absence of 4-1BB reduces obesity-induced atrophic response in skeletal muscle.
Article in Journal of inflammation (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Aerobic Exercise Attenuates High-Fat Diet-Induced Skeletal Muscle Atrophy by Suppressing Oxidative Stress, Inflammation, and Drp1-Associated Mitochondrial Fission.Antioxidants (Basel, Switzerland) · 2026Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
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Abstract
Obesity-induced inflammation causes skeletal muscle atrophy accompanied by disruption of oxidative metabolism and is implicated in metabolic complications such as insulin resistance and type 2 diabetes. We previously reported that 4-1BB, a member of the tumor necrosis factor receptor superfamily, participated in obesity-induced skeletal muscle inflammation. Here, we show that the absence of 4-1BB in obese mice fed a high-fat diet led to a decrease in expression of atrophic factors (MuRF1 and Atrogin-1) with suppression of NF-κB activity, and that this was accompanied by increases in mitochondrial oxidative metabolic genes/proteins (e.g., PGC-1α, CPT1β, etc.) expression and oxidative muscle fibers marker genes/proteins in the skeletal muscle. These findings suggest that 4-1BB-mediated inflammatory signaling could be a potential target for combating obesity-related muscle atrophy and metabolic derangement in skeletal muscle.
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