ArticleBiochemical and biophysical research communications2014
The TWEAK-Fn14 dyad is involved in age-associated pathological changes in skeletal muscle.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Circulating factors associated with sarcopenia during ageing and after intensive lifestyle intervention.Journal of cachexia, sarcopenia and muscle · 2019Trial
- Targeting TWEAK to enhance mitochondrial biogenesis and attenuate age-related muscle mass loss.Scientific reports · 2026Article
- TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence.Future science OA · 2025Article
- Advanced High-Content Phenotypic Screening to Identify Drugs That Ameliorate the Inhibition of Skeletal Muscle Cell Differentiation Induced by Cancer Cachexia Serum.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Melatonin Ameliorates Age-Related Sarcopenia via the Gut-Muscle Axis Mediated by Serum Lipopolysaccharide and Metabolites.Journal of cachexia, sarcopenia and muscle · 2025Article
- Chronic circadian misalignment accelerates sarcopenia progression in mice.Frontiers in physiology · 2025Article
- Potential therapeutic targets for sarcopenia identified by Mendelian randomisation.Age and ageing · 2023Article
- The inflammatory response, a mixed blessing for muscle homeostasis and plasticity.Frontiers in physiology · 2022Review
- Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix.Journal of developmental biology · 2021Article
- Emerging molecular mediators and targets for age-related skeletal muscle atrophy.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Aging-associated genesOncology letters · 2020Article
- TNFRSF12A and CD38 Contribute to a Vicious Circle for Chronic Obstructive Pulmonary Disease by Engaging Senescence Pathways.Frontiers in cell and developmental biology · 2020Article
- Genome-Wide Association Analysis With a 50K Transcribed Gene SNP-Chip Identifies QTL Affecting Muscle Yield in Rainbow Trout.Frontiers in genetics · 2018Article
- TWEAK/Fn14 Activation Participates in Skin Inflammation.Mediators of inflammation · 2017Review
- Emerging roles for histone deacetylases in age-related muscle atrophy.Nutrition and healthy aging · 2016Review
- Heightened TWEAK-NF-κB signaling and inflammation-associated fibrosis in paralyzed muscles of men with chronic spinal cord injury.American journal of physiology. Endocrinology and metabolism · 2016Article
- Article
- Elevated levels of TWEAK in skeletal muscle promote visceral obesity, insulin resistance, and metabolic dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Fn14, a Downstream Target of the TGF-β Signaling Pathway, Regulates Fibroblast Activation.PloS one · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive loss of skeletal muscle mass and strength (sarcopenia) is a major clinical problem in the elderly. Recently, proinflammatory cytokine TWEAK and its receptor Fn14 were identified as key mediators of muscle wasting in various catabolic states. However, the role of the TWEAK-Fn14 pathway in pathological changes in skeletal muscle during aging remains unknown. In this study, we demonstrate that the levels of Fn14 are increased in skeletal muscle of 18-month old (aged) mice compared with adult mice. Genetic ablation of Fn14 significantly increased the levels of specific muscle proteins and blunted the age-associated fiber atrophy in mice. While gene expression of two prominent muscle-specific E3 ubiquitin ligases MAFBx and MuRF1 remained comparable, levels of ubiquitinated proteins and the expression of autophagy-related molecule Atg12 were significantly reduced in Fn14-knockout (KO) mice compared with wild-type mice during aging. Ablation of Fn14 significantly diminished the DNA-binding activity of transcription factor nuclear factor-kappa B (NF-κB), gene expression of various inflammatory molecules, and interstitial fibrosis in skeletal muscle of aged mice. Collectively, our study suggests that the TWEAK-Fn14 signaling axis contributes to age-associated muscle atrophy and fibrosis potentially through its local activation of proteolytic systems and inflammatory pathways.
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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.