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Related Concept Videos

Formation of Muscle Fibers from Myoblasts01:13

Formation of Muscle Fibers from Myoblasts

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De novo myogenesis, or the formation of muscle fibers, begins during the early embryonic stages. The skeletal muscle is formed from somites– blocks of embryonic cell layers. The somites are further divided into dermatomes, myotomes, sclerotomes, and syndetomes. Among these, the myotomes give rise to muscle fibers.
Muscle progenitor cells (MPCs) are formed from the myotomes. MPCs express genes that encode the transcription factors Pax3 and Pax7. Along with Pax 3/7, other transcription...
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The Neuromuscular Junction01:19

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The nervous system consists of complex motor neuron circuits, including upper motor neurons originating from the cerebral cortex and lower motor neurons starting in the spinal cord, coordinating both voluntary and involuntary movements. Among these, somatic motor neurons activate skeletal muscles and are classified into alpha, beta, and gamma types. Alpha neurons are vital for voluntary movement coordination, while gamma neurons adjust muscle spindle sensitivity, and the function of beta...
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Excitation-Contraction Coupling in Skeletal Muscles01:20

Excitation-Contraction Coupling in Skeletal Muscles

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Excitation-contraction coupling is a series of events that occur between generating an action potential and initiating a muscle contraction. It occurs at the triad, a structure found in skeletal muscle fibers that comprise a T-tubule and terminal cisternae of the sarcoplasmic reticulum on each side. These triads are visible in longitudinally sectioned muscle fibers. They are typically located at the A-I junction — the junction between the A and I bands of the sarcomere.
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The Sarcomere01:08

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A sarcomere is a microscopic segment repeating in a myofibril. The sarcomere fundamentally consists of two main myofilaments: thick filaments called myosin and thin filaments called actin. These filaments interact by sliding past each other in response to stimulus. In addition to myosin and actin, several other proteins, such as tropomyosin, troponin, titin, nebulin, myomesin, α-actinin, and dystrophin, play crucial roles in regulating, structuring, and functioning of the sarcomere.
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Satellite Stem Cells and Muscular Dystrophy01:21

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Satellite stem cells or myosatellite cells are quiescent stem cells that Alexander Mauro first identified in 1961. These cells are located between the sarcolemma, the plasma membrane of muscle fibers, and the basal lamina, the connective tissue sheath covering it. These mononucleated cells are activated in response to muscle injury, can transform into myoblasts, and may form or repair muscle fibers. Myosatellite cells can provide additional myonuclei for muscle regeneration or return to a...
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Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

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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.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open....
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Related Experiment Video

Updated: May 7, 2026

Dissection of Single Skeletal Muscle Fibers for Immunofluorescent and Morphometric Analyses of Whole-Mount Neuromuscular Junctions
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Dissection of Single Skeletal Muscle Fibers for Immunofluorescent and Morphometric Analyses of Whole-Mount Neuromuscular Junctions

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Myotendinous Junction development and repair.

Kun Yang1,2, Zi Yin2, Chunmei Fan3,1,4

  • 1Department of Sports Medicine & Orthopedic Surgery, The Second Affiliated Hospital, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.

Journal of Orthopaedic Translation
|May 6, 2026
PubMed
Summary
This summary is machine-generated.

This review synthesizes myotendinous junction (MTJ) development and repair, highlighting suboptimal outcomes. Integrating developmental insights, stem/progenitor cells, and regulatory signals via tissue engineering offers enhanced MTJ regeneration strategies.

Keywords:
CytoskeletonDevelopmentExtracellular matrixMyotendinous junctionRepairStem/progenitor cell

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Author Spotlight: Advancing Tendon Research by Developing Mouse Assembloids to Understand Cellular Mechanisms
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Author Spotlight: Advancing Tendon Research by Developing Mouse Assembloids to Understand Cellular Mechanisms

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Area of Science:

  • Myotendinous junction (MTJ) structure and function.
  • Muscle-tendon interface biology.
  • Regenerative medicine and tissue engineering.

Background:

  • The myotendinous junction (MTJ) is crucial for movement and a common injury site.
  • Current MTJ repair strategies yield suboptimal outcomes due to limited understanding of MTJ development.
  • A comprehensive synthesis of MTJ structure, cellular components, and developmental mechanisms is needed for effective regeneration.

Purpose of the Study:

  • To synthesize current knowledge on MTJ structure, cellular diversity, and developmental mechanisms.
  • To evaluate existing MTJ repair strategies in light of developmental insights.
  • To propose enhanced tissue engineering approaches for MTJ repair.

Main Methods:

  • Review of existing literature on MTJ development, maintenance, and repair.
  • Analysis of cytoskeletal and extracellular matrix (ECM) architecture.
  • Identification of key cell types and molecular regulators (e.g., Slit, LRT, BMP4).
  • Evaluation of current and emerging MTJ repair strategies.

Main Results:

  • The MTJ possesses a hierarchical architecture with specific molecular complexes mediating muscle-tendon connection.
  • Col22a1-expressing muscle nuclei and resident stem/progenitor cells play vital roles in MTJ maintenance and healing.
  • Existing treatments often neglect crucial developmental aspects, particularly stem/progenitor cells and regulatory signals.

Conclusions:

  • Tissue engineering integrating MTJ-resident stem/progenitor cells (e.g., CD106+CD24- MTPs, Hic1+Col22a1+ progenitors) and key regulatory signals (Slit, Lrt, BMP4) can significantly improve MTJ repair efficacy.
  • Developing MTJ organoids can accelerate drug testing for MTJ injuries.
  • Standardizing conventional treatments and advancing large-animal validation for emerging therapies are crucial for clinical translation.