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Related Concept Videos

Classification of Skeletal Muscle Fibers01:48

Classification of Skeletal Muscle Fibers

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Skeletal muscles continuously produce ATP to provide the energy that enables muscle contractions. Skeletal muscle fibers can be categorized into three types based on differences in their contraction speed and how they produce ATP, as well as physical differences related to these factors. Most human muscles contain all three muscle fiber types, albeit in varying proportions.
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Slow oxidative, muscle fibers appear red due to large numbers of capillaries and high levels of...
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A type of Lewis acid-base chemistry involves the formation of a complex ion (or a coordination complex) comprising a central atom, typically a transition metal cation, surrounded by ions or molecules called ligands. These ligands can be neutral molecules like H2O or NH3, or ions such as CN− or OH−. Often, the ligands act as Lewis bases, donating a pair of electrons to the central atom. These types of Lewis acid-base reactions are examples of a broad subdiscipline called coordination...
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Skeletal muscles are composed of a bundle of muscle fibers and are attached to bones through tendons. Each skeletal muscle fiber is a single muscle cell. The sarcolemma, the plasma membrane of a skeletal muscle cell, consists of a lipid bilayer and glycocalyx that supports muscle fibers. The sarcolemma extends into the muscle cells to form tubular structures called transverse or T-tubules. Each side of the T-tubules consists of a membrane-bound structure called the sarcoplasmic reticulum,...
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The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
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The naming of the approximately 700 muscles in the human body is based on a set of criteria designed to provide descriptive information about each muscle, making it easier to identify and remember them.
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Related Experiment Video

Updated: Jan 29, 2026

Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice
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Inhibition of TRPC3-Nox2 Complex Formation Ameliorates Skeletal Muscle Atrophy.

Yuri Kato1, Di Wu1, Tomoya Ito1

  • 1Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.

Antioxidants (Basel, Switzerland)
|January 28, 2026
PubMed
Summary

The protein complex between transient receptor potential canonical 3 (TRPC3) and NADPH oxidase 2 (Nox2) drives skeletal muscle atrophy. Disrupting this complex may offer a therapeutic strategy for Duchenne muscular dystrophy (DMD).

Keywords:
Nox2TRPC3protein–protein interactionskeletal muscle atrophy

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Area of Science:

  • Molecular Biology
  • Muscle Physiology
  • Oxidative Stress Research

Background:

  • Skeletal muscle atrophy is linked to sarcopenia, frailty, and muscular dystrophies.
  • The molecular mechanisms connecting oxidative stress to muscle degeneration are not fully understood.
  • Previous work identified a TRPC3-Nox2 complex driving heart muscle atrophy.

Purpose of the Study:

  • To investigate the role of the TRPC3-Nox2 complex in skeletal muscle wasting.
  • To determine if targeting this complex could be a therapeutic strategy for muscle atrophy.

Main Methods:

  • Examined TRPC3-Nox2 complex formation in mouse models of denervation and Duchenne muscular dystrophy (mdx).
  • Utilized TRPC3 deletion, pharmacological inhibitors, and AAV-mediated gene therapy.
  • Assessed muscle atrophy (cross-sectional area), reactive oxygen species (ROS) production, muscle strength, and plasma creatine kinase levels.

Main Results:

  • TRPC3-Nox2 complex formation was enhanced in skeletal muscle of denervated and mdx mice.
  • TRPC3 deletion reduced denervation-induced atrophy and ROS production.
  • Pharmacological and genetic disruption of the TRPC3-Nox2 complex showed potential in mitigating muscle wasting in mdx mice.

Conclusions:

  • TRPC3-Nox2 complex formation is a key driver of oxidative stress-mediated skeletal muscle atrophy.
  • Targeting the TRPC3-Nox2 interaction presents a potential therapeutic avenue for Duchenne muscular dystrophy and other muscle-wasting disorders.