ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
MyD88-mediated signaling intercedes in neurogenic muscle atrophy through multiple mechanisms.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Spatial-Bioenergetic-Immune Axis in Type 2 Diabetes Mellitus-Associated Sarcopenia: A Review from Pathogenesis to Targeted Reconstruction.Journal of inflammation research · 2026Review
- Effect of NF-κB on Myosin Heavy Chain Content and Muscle Atrophy After Laryngeal Muscle Denervation.World journal of otorhinolaryngology - head and neck surgery · 2025Article
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Transcriptome sequencing analysis reveals the molecular mechanism of sepsis-induced muscle atrophy.Journal of thoracic disease · 2024Article
- Ammonia transporter RhBG initiates downstream signaling and functional responses by activating NFκB.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Deubiquitinases in muscle physiology and disorders.Biochemical Society transactions · 2024Review
- Emerging role of TAK1 in the regulation of skeletal muscle mass.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- Delayed denervation-induced muscle atrophy inFrontiers in physiology · 2023Article
- Inflammaging: Implications in Sarcopenia.International journal of molecular sciences · 2022Review
- Functional Nutrients to Ameliorate Neurogenic Muscle Atrophy.Metabolites · 2022Review
- Article
- Hidden Agenda - The Involvement of Endoplasmic Reticulum Stress and Unfolded Protein Response in Inflammation-Induced Muscle Wasting.Frontiers in immunology · 2022Review
- Effect of Denervation on XBP1 in Skeletal Muscle and the Neuromuscular Junction.International journal of molecular sciences · 2021Article
- The IRE1/XBP1 signaling axis promotes skeletal muscle regeneration through a cell non-autonomous mechanism.eLife · 2021Article
- Strategies for Biomaterial-Based Spinal Cord Injury RepairFrontiers in bioengineering and biotechnology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle atrophy is a debilitating complication of many chronic disease states and disuse conditions including denervation. However, molecular and signaling mechanisms of muscle wasting remain less understood. Here, we demonstrate that the levels of several toll-like receptors (TLRs) and their downstream signaling adaptor, myeloid differentiation primary response 88 (MyD88), are induced in skeletal muscle of mice in response to sciatic nerve denervation. Muscle-specific ablation of MyD88 mitigates denervation-induced skeletal muscle atrophy in mice. Targeted ablation of MyD88 suppresses the components of ubiquitin-proteasome system, autophagy, and FOXO transcription factors in skeletal muscle during denervation. We also found that specific inhibition of MyD88 reduces the activation of canonical nuclear factor-kappa (NF-κB) pathway and expression of receptors for inflammatory cytokines in denervated muscle. In contrast, inhibition of MyD88 stimulates the activation of non-canonical NF-κB signaling in denervated skeletal muscle. Ablation of MyD88 also inhibits the denervation-induced increase in phosphorylation of AMPK without having any effect on the phosphorylation of mTOR. Moreover, targeted ablation of MyD88 inhibits the activation of a few components of the unfolded protein response (UPR) pathways, especially X-box protein 1 (XBP1). Importantly, myofiber-specific ablation of XBP1 mitigates denervation-induced skeletal muscle atrophy in mice. Collectively, our experiments suggest that TLR-MyD88 signaling mediates skeletal muscle wasting during denervation potentially through the activation of canonical NF-κB signaling, AMPK and UPR pathways.
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