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Thyroid Hormone Action in Muscle Atrophy.

Maria Angela De Stefano1, Raffaele Ambrosio2, Tommaso Porcelli3

  • 1Department of Clinical Medicine and Surgery, University of Naples Federico II, 80131 Naples, Italy.

Metabolites
|November 25, 2021
PubMed
Summary

Thyroid hormone (TH) impacts skeletal muscle atrophy by altering protein turnover. Modulating deiodinase enzymes, which control intracellular TH levels, may offer a therapeutic strategy for muscle wasting conditions.

Keywords:
deiodinasemuscle atrophythyroid hormone

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Area of Science:

  • Endocrinology
  • Muscle Physiology
  • Molecular Biology

Background:

  • Skeletal muscle atrophy involves excessive protein degradation, leading to muscle mass loss and weakness.
  • Thyroid hormone (TH) is crucial in skeletal muscle, regulating growth and metabolism.
  • Intracellular TH levels are controlled by deiodinase enzymes (D2 and D3) in muscle.

Purpose of the Study:

  • To review the role of TH in skeletal muscle atrophy.
  • To explore molecular mechanisms controlling intracellular T3 concentration during muscle wasting.
  • To discuss deiodinase modulation as a potential therapeutic approach.

Main Methods:

  • Literature review of thyroid hormone action in skeletal muscle atrophy.
  • Analysis of molecular mechanisms regulating deiodinases in muscle wasting.
  • Discussion of therapeutic strategies targeting deiodinases.

Main Results:

  • TH influences protein synthesis and degradation in skeletal muscle.
  • Altered TH levels can cause myopathies.
  • Deiodinases D2 and D3 actively regulate intracellular T3 availability in muscle.

Conclusions:

  • Understanding TH's role in muscle atrophy is key.
  • Deiodinases are critical regulators of intracellular TH in atrophying muscle.
  • Targeting deiodinases presents a promising therapeutic avenue for muscle atrophy.