Overexpression of thioredoxin‐2 attenuates age‐related muscle loss by suppressing mitochondrial oxidative stress and apoptosis

Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age‐dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin‐2 (TXN2).

• Publication year

  2022

• Venue

  JCSM Rapid Communications

• Publication date

  2022-01-14

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/rco2.57PMID 40236683PMCID 11995840
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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