ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012
Pathways of Ca²⁺ entry and cytoskeletal damage following eccentric contractions in mouse skeletal muscle.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Eccentric and concentric blood flow restriction resistance training on indices of delayed onset muscle soreness in untrained women.European journal of applied physiology · 2019Trial
- Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026Review
- Skeletal muscle-specific PGC-1α-b overexpression prevents eccentric contraction-induced muscle injury through an utrophin-independent pathway in mice.Physiological reports · 2026Article
- Arginine ingestion inhibits phagocyte invasion in eccentrically contracted rat fast-twitch muscle.Journal of muscle research and cell motility · 2024Article
- The Effects of Antioxidant Supplementation on Soccer Performance and Recovery: A Critical Review of the Available Evidence.Nutrients · 2024Review
- Review
- Time-of-day effects on ex vivo muscle contractility following short-term satellite cell ablation.American journal of physiology. Cell physiology · 2024Article
- Re‑examining the mechanism of eccentric exercise‑induced skeletal muscle damage from the role of the third filament, titin (Review).Biomedical reports · 2024Review
- SERCA1 Overexpression in Skeletal Muscle Attenuates Muscle Atrophy and Improves Motor Function in a Mouse Model of ALS.Journal of neuromuscular diseases · 2024Article
- Harmonizing Magnetic Mitohormetic Regenerative Strategies: Developmental Implications of a Calcium-Mitochondrial Axis Invoked by Magnetic Field Exposure.Bioengineering (Basel, Switzerland) · 2023Review
- Blood Flow Restriction Attenuates Muscle Damage in Resistance Exercise Performed Until Concentric Muscle Failure.International journal of exercise science · 2023Article
- Mechanisms of eccentric contraction-induced muscle damage and nutritional supplementations for mitigating it.Journal of muscle research and cell motility · 2022Review
- TRPC channels in exercise-mimetic therapy.Pflugers Archiv : European journal of physiology · 2019Review
- Role of STIM1/ORAI1-mediated store-operated CaCell calcium · 2018Review
- Past injurious exercise attenuates activation of primary calcium-dependent injury pathways in skeletal muscle during subsequent exercise.Physiological reports · 2018Article
- Resistance exercise-induced muscle fatigue is not accompanied by increased phosphorylation of ryanodine receptor 1 at serine 2843.PloS one · 2018Article
- l-arginine ingestion inhibits eccentric contraction-induced proteolysis and force deficit via S-nitrosylation of calpain.Physiological reports · 2018Article
- Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading-induced atrophy.The Journal of physiology · 2016Article
- Icaritin requires Phosphatidylinositol 3 kinase (PI3K)/Akt signaling to counteract skeletal muscle atrophy following mechanical unloading.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscles that are stretched during contraction (eccentric contractions) show deficits in force production and a variety of structural changes, including loss of antibody staining of cytoskeletal proteins. Extracellular Ca(2+) entry and activation of calpains have been proposed as mechanisms involved in these changes. The present study used isolated mouse extensor digitorum longus (EDL) muscles subjected to 10 eccentric contractions and monitored force production, immunostaining of cytoskeletal proteins, and resting stiffness. Possible pathways for Ca(2+) entry were tested with streptomycin (200 μM), a blocker of stretch-activated channels, and with muscles from mice deficient in the transient receptor potential canonical 1 gene (TRPC1 KO), a candidate gene for stretch-activated channels. At 30 min after the eccentric contractions, the isometric force was decreased to 75 ± 3% of initial control and this force loss was reduced by streptomycin but not in the TRPC1 KO. Desmin, titin, and dystrophin all showed patchy loss of immunostaining 30 min after the eccentric contractions, which was substantially reduced by streptomycin and in the TRPC1 KO muscles. Muscles showed a reduction of resting stiffness following eccentric contractions, and this reduction was eliminated by streptomycin and absent in the TRPC1 KO muscles. Calpain activation was determined by the appearance of a lower molecular weight autolysis product and μ-calpain was activated at 30 min, whereas the muscle-specific calpain-3 was not. To test whether the loss of stiffness was caused by titin cleavage, protein gels were used but no significant titin cleavage was detected. These results suggest that Ca(2+) entry following eccentric contractions is through a stretch-activated channel that is blocked by streptomycin and encoded or modulated by TRPC1.
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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.