ReviewFrontiers in immunology2014
TWEAK/Fn14 Signaling Axis Mediates Skeletal Muscle Atrophy and Metabolic Dysfunction.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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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
43 citing papers in PubMed, 72 citations in OpenAlex.
- Perioperative assessment of muscle inflammation susceptibility in patients with end-stage osteoarthritis.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Trial
- Human skeletal muscle macrophages increase following cycle training and are associated with adaptations that may facilitate growth.Scientific reports · 2019Trial
- Disruptions of cell signaling pathways in myotonic dystrophy type 1 skeletal muscle, their pathogenic impact, and potential for combinatorial therapeutics.The Journal of biological chemistry · 2026Review
- Recreational Exercise and Inflammatory Patterns in Hashimoto's Thyroiditis: Observations from a Cross-Sectional Study.Biomolecules · 2025Observational
- Article
- Multi-Omics Identification ofBiology · 2025Article
- Exercise, disease state and sex influence the beneficial effects of Fn14-depletion on survival and muscle pathology in the SOD1Skeletal muscle · 2024Article
- The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.Cancer cell · 2024Article
- Exercise microdosing for skeletal muscle health applications to spaceflight.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Human skeletal muscle aging atlas.Nature aging · 2024Article
- Systemic Markers of Lung Function and Forced Expiratory Volume in 1 Second Decline across Diverse Cohorts.Annals of the American Thoracic Society · 2023Article
- Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.Frontiers in nutrition · 2023Review
- Targeted ablation of Fn14 receptor improves exercise capacity and inhibits neurogenic muscle atrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Dysregulation of Tweak and Fn14 in skeletal muscle of spinal muscular atrophy mice.Skeletal muscle · 2022Article
- Mechanisms of exercise as a preventative measure to muscle wasting.American journal of physiology. Cell physiology · 2021Review
- Transcriptome profiling of the diaphragm in a controlled mechanical ventilation model reveals key genes involved in ventilator-induced diaphragmatic dysfunction.BMC genomics · 2021Article
- Regulation of dynamin-related protein 1 (DRP1) levels modulates myoblast atrophy induced by C26 colon cancer-conditioned medium.Translational cancer research · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- A reference single-cell transcriptomic atlas of human skeletal muscle tissue reveals bifurcated muscle stem cell populations.Skeletal muscle · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) through binding to its receptor fibroblast growth factor inducible 14 (Fn14) has been shown to regulate many cellular responses including proliferation, differentiation, apoptosis, inflammation, and fibrosis, under both physiological and pathological conditions. Emerging evidence suggests that TWEAK is also a major muscle wasting cytokine. TWEAK activates nuclear factor-κB signaling and proteolytic pathways such as ubiquitin-proteasome system, autophagy, and caspases to induce muscle proteolysis in cultured myotubes. Fn14 is dormant or expressed in minimal amounts in normal healthy muscle. However, specific atrophic conditions, such as denervation, immobilization, and starvation stimulate the expression of Fn14 leading to activation of TWEAK/Fn14 signaling and eventually skeletal muscle atrophy. TWEAK also causes slow- to fast-type fiber transition in skeletal muscle. Furthermore, recent studies suggest that TWEAK diminishes mitochondrial content and represses skeletal muscle oxidative phosphorylation capacity. TWEAK mediates these effects through affecting the expression of a number of genes and microRNAs. In this review article, we have discussed the recent advancements toward understanding the role and mechanisms of action of TWEAK/Fn14 signaling in skeletal muscle with particular reference to different models of atrophy and oxidative metabolism.
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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.