ArticleAmerican journal of physiology. Endocrinology and metabolism2016
Heightened TWEAK-NF-κB signaling and inflammation-associated fibrosis in paralyzed muscles of men with chronic spinal cord injury.
Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
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Who cites it
31 citing papers in PubMed, 36 citations in OpenAlex.
- The Effect of Lower Limb Combined Neuromuscular Electrical Stimulation on Skeletal Muscle Signaling for Glucose Utilization, Myofiber Distribution, and Metabolic Function after Spinal Cord Injury.International journal of environmental research and public health · 2023Trial
- Perioperative assessment of muscle inflammation susceptibility in patients with end-stage osteoarthritis.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Trial
- Muscle Fn14 gene expression is associated with fat-free mass retention during energy deficit at high altitude.Physiological reports · 2018Trial
- Biochemical Biomarker Combinations in Human Traumatic Spinal Cord Injury: An Exploratory Study.Journal of clinical medicine · 2026Article
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- Article
- The Effect of Lower Limb Combined Neuromuscular Electrical Stimulation on Skeletal Muscle Cross-Sectional Area and Inflammatory Signaling.International journal of molecular sciences · 2024Article
- Transcriptomics reveals transient and dynamic muscle fibrosis and atrophy differences following spinal cord injury in rats.Journal of cachexia, sarcopenia and muscle · 2024Article
- The shared molecular mechanism of spinal cord injury and sarcopenia: a comprehensive genomics analysis.Frontiers in neurology · 2024Article
- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 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
- Muscle transcriptomic circuits linked to periarticular physiology in end-stage osteoarthritis.Physiological genomics · 2022Article
- TNF-like weak inducer of apoptosis / nuclear factor κB axis feedback loop promotes spinal cord injury by inducing astrocyte activation.Bioengineered · 2022Article
- Review
- Pharmacologic approaches to prevent skeletal muscle atrophy after spinal cord injury.Current opinion in pharmacology · 2021Review
- Mechanisms of exercise as a preventative measure to muscle wasting.American journal of physiology. Cell physiology · 2021Review
- The Repression of the HMGB1-TLR4-NF-κB Signaling Pathway by Safflower Yellow May Improve Spinal Cord Injury.Frontiers in neuroscience · 2021Review
- MuRF1/TRIM63, Master Regulator of Muscle Mass.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Individuals with long-standing spinal cord injury (SCI) often present with extreme muscle atrophy and impaired glucose metabolism at both the skeletal muscle and whole body level. Persistent inflammation and increased levels of proinflammatory cytokines in the skeletal muscle are potential contributors to dysregulation of glucose metabolism and atrophy; however, to date no study has assessed the effects of long-standing SCI on their expression or intracellular signaling in the paralyzed muscle. In the present study, we assessed the expression of genes (TNFαR, TNFα, IL-6R, IL-6, TWEAK, TWEAK R, atrogin-1, and MuRF1) and abundance of intracellular signaling proteins (TWEAK, TWEAK R, NF-κB, and p-p65/p-50/105) that are known to mediate inflammation and atrophy in skeletal muscle. In addition, based on the effects of muscle inflammation on promotion of skeletal muscle fibrosis, we assessed the degree of fibrosis between myofibers and fascicles in both groups. For further insight into the distribution and variability of muscle fiber size, we also analyzed the frequency distribution of SCI fiber size. Resting vastus lateralis (VL) muscle biopsy samples were taken from 11 men with long-standing SCI (≈22 yr) and compared with VL samples from 11 able-bodied men of similar age. Our results demonstrated that chronic SCI muscle has heightened TNFαR and TWEAK R gene expression and NF-κB signaling (higher TWEAK R and phospho-NF-κB p65) and fibrosis, along with substantial myofiber size heterogeneity, compared with able-bodied individuals. Our data suggest that the TWEAK/TWEAK R/NF-κB signaling pathway may be an important mediator of chronic inflammation and fibrotic adaptation in SCI muscle.
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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.