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Related Concept Videos

Mitochondria01:37

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased...
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
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Updated: Jul 21, 2025

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Mitochondrial dysfunction: roles in skeletal muscle atrophy.

Xin Chen1, Yanan Ji1, Ruiqi Liu2

  • 1Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Department of Neurology, Affiliated Hospital of Nantong University, Nantong University, Nantong, 226001, Jiangsu, People's Republic of China.

Journal of Translational Medicine
|July 26, 2023
PubMed
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Mitochondrial dysfunction contributes to skeletal muscle atrophy. This review explores its mechanisms and therapeutic strategies, including drugs, exercise, and gene therapy, for muscle health.

Keywords:
AntioxidantsMitochondrial dysfunctionMuscle atrophyTherapy

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Area of Science:

  • Cellular Biology
  • Physiology
  • Biochemistry

Background:

  • Mitochondria are crucial for skeletal muscle homeostasis and health.
  • Mitochondrial damage and dysfunction precipitate pathophysiological changes, including muscle atrophy.
  • The molecular mechanisms underlying mitochondrial dysfunction in skeletal muscle atrophy are intricate.

Purpose of the Study:

  • To elucidate the role of mitochondria in skeletal muscle.
  • To describe the impact of mitochondrial dysfunction on skeletal muscle atrophy and its molecular underpinnings.
  • To review therapeutic strategies targeting mitochondrial function for muscle atrophy.

Main Methods:

  • Literature review of mitochondrial roles in skeletal muscle.
  • Analysis of molecular mechanisms linking mitochondrial dysfunction to muscle atrophy.
  • Investigation of signaling pathways (e.g., AMPK-SIRT1-PGC-1α, IGF-1-PI3K-Akt-mTOR) and mitochondrial factors.
  • Examination of mitochondrial dysfunction manifestations in disease-induced muscle atrophy.
  • Summary of therapeutic interventions.

Main Results:

  • Mitochondrial dysfunction significantly impacts skeletal muscle atrophy.
  • Various signaling pathways and mitochondrial factors are implicated in the pathogenesis.
  • Mitochondrial dysfunction is observed across different diseases causing muscle atrophy.
  • Targeted regulation of mitochondrial function shows promise in prevention and treatment.

Conclusions:

  • Understanding mitochondrial dysfunction is key to preventing and treating skeletal muscle atrophy.
  • Targeting mitochondrial function offers a promising therapeutic avenue for muscle atrophy.
  • This review provides a comprehensive overview for future research and therapeutic development.