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Related Concept Videos

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

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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 site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
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Mitophagy in Botulinum Toxin Type A-Induced Muscle Atrophy.

Qian-Ying Mao1, Zhuo Chen2, Shang Xie1

  • 1Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.

Oral Diseases
|December 13, 2025
PubMed
Summary
This summary is machine-generated.

Botulinum toxin type A (BTXA) causes masseter muscle atrophy by activating mitophagy, a process crucial for muscle homeostasis. This study reveals mitophagy as a key mechanism in BTXA-induced muscle changes.

Keywords:
botulinum toxin type Amasseter musclemitophagymuscle atrophy

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Area of Science:

  • Muscle physiology
  • Cellular biology
  • Biochemistry

Background:

  • Botulinum toxin type A (BTXA) is used in oral surgery for masseter hypertrophy and bruxism.
  • BTXA induces transient masseter atrophy, but the mechanism is unclear.
  • Mitophagy is vital for muscle homeostasis and atrophy.

Purpose of the Study:

  • To investigate if mitophagy mediates BTXA-induced masseter muscle atrophy.
  • To understand the cellular mechanisms behind BTXA's effects on the masseter muscle.

Main Methods:

  • Rats received BTXA injections.
  • Assessed muscle fiber composition using histology and immunofluorescence.
  • Quantified mitophagy markers (LC3-II, p62, beclin-1, Tomm20) via western blot.
  • Evaluated mitochondrial function through ATP content and mtDNA copy number.

Main Results:

  • BTXA induced transient masseter atrophy with altered muscle fiber types (increased IIA, decreased IIB).
  • Mitophagy markers LC3-II, p62, and beclin-1 were upregulated; Tomm20 was downregulated at 2 weeks.
  • Impaired mitochondrial function was indicated by reduced ATP content and mtDNA copy number.

Conclusions:

  • Mitophagy plays a critical role in BTXA-induced masseter muscle atrophy.
  • These findings offer new insights into the mechanisms of BTXA treatment in oral and maxillofacial surgery.