ArticleFrontiers in physiology2022
Long-Lasting Impairments in Quadriceps Mitochondrial Health, Muscle Size, and Phenotypic Composition Are Present After Non-invasive Anterior Cruciate Ligament Injury.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Structural determinants of quadriceps atrophy following ACL injury: Evidence for fibre atrophy without fibre loss or overt peripheral denervation.The Journal of physiology · 2026Article
- ACL injury reprograms quadriceps myonuclear epigenetic and transcriptional signatures in mice.Molecular medicine (Cambridge, Mass.) · 2026Article
- Knee Health Is a Major Determinant of Mobility Across the Healthspan.Journal of functional morphology and kinesiology · 2025Review
- Redox signaling‑mediated muscle atrophy in ACL injury: Role of physical exercise (Review).Molecular medicine reports · 2025Review
- Overexpression of manganese superoxide dismutase mitigates ACL injury-induced muscle atrophy, weakness and oxidative damage.Free radical biology & medicine · 2024Article
- Quadriceps muscle atrophy after non-invasive anterior cruciate ligament injury: evidence linking to autophagy and mitophagy.Frontiers in physiology · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
introductionDespite rigorous rehabilitation aimed at restoring muscle health, anterior cruciate ligament (ACL) injury is often hallmarked by significant long-term quadriceps muscle weakness. Derangements in mitochondrial function are a common feature of various atrophying conditions, yet it is unclear to what extent mitochondria are involved in the detrimental sequela of quadriceps dysfunction after ACL injury. Using a preclinical, non-invasive ACL injury rodent model, our objective was to explore the direct effect of an isolated ACL injury on mitochondrial function, muscle atrophy, and muscle phenotypic transitions.
methodsA total of 40 male and female, Long Evans rats (16-week-old) were exposed to non-invasive ACL injury, while 8 additional rats served as controls. Rats were euthanized at 3, 7, 14, 28, and 56 days after ACL injury, and vastus lateralis muscles were extracted to measure the mitochondrial respiratory control ratio (RCR; state 3 respiration/state 4 respiration), mitochondrial reactive oxygen species (ROS) production, fiber cross sectional area (CSA), and fiber phenotyping. Alterations in mitochondrial function and ROS production were detected using two-way (sex:group) analyses of variance. To determine if mitochondrial characteristics were related to fiber atrophy, individual linear mixed effect models were run by sex.
resultsMitochondria-derived ROS increased from days 7 to 56 after ACL injury (30-100%,
conclusionLong-lasting impairments in quadriceps mitochondrial health are present after ACL injury and play a key role in the dysregulation of quadriceps muscle size and composition. Our preclinical data indicate that using mitoprotective therapies may be a potential therapeutic strategy to mitigate alterations in muscle size and characteristic after ACL injury.
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