ArticleAmerican journal of physiology. Cell physiology2010
Role of TRPC1 channel in skeletal muscle function.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 118 citations in OpenAlex.
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- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- Piezo1 Regulates the Skeletal Muscle Length-Tension Relationship Through Channel-Independent Mechanotransduction.Biomolecules · 2026Article
- Mechanical memory of excitable cells induced by mechanosensitive channel inactivation.Biophysical journal · 2025Article
- Brief Weekly Magnetic Field Exposure Enhances Avian Oxidative Muscle Character During Embryonic Development.International journal of molecular sciences · 2025Article
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- TRPC1 links calcium signaling to cellular senescence in the protection against posttraumatic osteoarthritis.JCI insight · 2024Article
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- Cyclo His-Pro Attenuates Muscle Degeneration in Murine Myopathy Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The emerging role of Piezo1 channels in skeletal muscle physiology.Biophysical reviews · 2023Review
- The Developmental Implications of Muscle-Targeted Magnetic Mitohormesis: A Human Health and Longevity Perspective.Bioengineering (Basel, Switzerland) · 2023Review
- Article
- Mechanotransduction for Muscle Protein Synthesis via Mechanically Activated Ion Channels.Life (Basel, Switzerland) · 2023Review
- Biomechanical, Microstructural and Material Properties of Tendon and Bone in the Young Oim Mice Model of Osteogenesis Imperfecta.International journal of molecular sciences · 2022Article
- Review
- Inhibition of sphingolipid de novo synthesis counteracts muscular dystrophy.Science advances · 2022Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Ion Channels and Transporters in Muscle Cell Differentiation.International journal of molecular sciences · 2021Review
- Calsequestrin 1 Is an Active Partner of Stromal Interaction Molecule 2 in Skeletal Muscle.Cells · 2021Article
- Function of the PorcineCells · 2021Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu, excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+ is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+ and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1(-/-) mice. The influx of Ca2+ through TRPC1 channels represents a minor part of the entry of Ca(2+) into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+ concentration ([Ca2+](i)) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+ entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1(-/-) mice stimulated repeatedly progressively display lower [Ca2+](i) transients than those observed in TRPC1(+/+) fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1(-/-) mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1(-/-) mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca(2+) during repeated contractions and help muscles to maintain their force during sustained repeated contractions.
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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.