ArticleeLife2022
Tenotomy-induced muscle atrophy is sex-specific and independent of NFκB.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Loss of ovarian hormones modulates sex-specific metabolic adaptations to volumetric muscle loss.American journal of physiology. Cell physiology · 2026Article
- Prediabetes Associates With Musculoskeletal Alterations Independent of Total Body Adiposity.Journal of cachexia, sarcopenia and muscle · 2026Article
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Intramuscular adipose tissue: from progenitor to pathology.American journal of physiology. Cell physiology · 2025Review
- Oxygen-Ozone Therapy in Tendinopathy Management: A Comprehensive Review.Journal of personalized medicine · 2025Review
- Ablation of UCP-1+ cells impacts FAP dynamics in muscle regeneration.American journal of physiology. Cell physiology · 2025Article
- Time-of-day effects on muscle mitochondria following short-term ablation of satellite cells.Frontiers in physiology · 2025Article
- Transcriptional evidence for transient regulation of muscle regeneration by brown adipose transplant in the rotator cuff.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024Article
- Sexual dimorphisms in skeletal muscle: current concepts and research horizons.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Review
- Metformin mitigates adipogenesis of fibro-adipogenic progenitors after rotator cuff tears via activating mTOR/ULK1-mediated autophagy.American journal of physiology. Cell physiology · 2024Article
- Studying intramuscular fat deposition and muscle regeneration: insights from a comparative analysis of mouse strains, injury models, and sex differences.Skeletal muscle · 2024Article
- Rotator cuff tears.Nature reviews. Disease primers · 2024Review
- Skeletal muscle delimited myopathy and verapamil toxicity in SUR2 mutant mouse models of AIMS.EMBO molecular medicine · 2023Article
- Sex Differences in Inflammation and Muscle Wasting in Aging and Disease.International journal of molecular sciences · 2023Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The nuclear factor-κB (NFκB) pathway is a major thoroughfare for skeletal muscle atrophy and is driven by diverse stimuli. Targeted inhibition of NFκB through its canonical mediator IKKβ effectively mitigates loss of muscle mass across many conditions, from denervation to unloading to cancer. In this study, we used gain- and loss-of-function mouse models to examine the role of NFκB in muscle atrophy following rotator cuff tenotomy - a model of chronic rotator cuff tear. IKKβ was knocked down or constitutively activated in muscle-specific inducible transgenic mice to elicit a twofold gain or loss of NFκB signaling. Surprisingly, neither knockdown of IKKβ nor overexpression of caIKKβ significantly altered the loss of muscle mass following tenotomy. This finding was consistent across measures of morphological adaptation (fiber cross-sectional area, fiber length, fiber number), tissue pathology (fibrosis and fatty infiltration), and intracellular signaling (ubiquitin-proteasome, autophagy). Intriguingly, late-stage tenotomy-induced atrophy was exacerbated in male mice compared with female mice. This sex specificity was driven by ongoing decreases in fiber cross-sectional area, which paralleled the accumulation of large autophagic vesicles in male, but not female muscle. These findings suggest that tenotomy-induced atrophy is not dependent on NFκB and instead may be regulated by autophagy in a sex-specific manner.
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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.