ArticleMuscles (Basel, Switzerland)2023
Degradative Signaling in ATG7-Deficient Skeletal Muscle Following Cardiotoxin Injury.
Article in Muscles (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Physiological medium and 3-hydroxybutyrate modulate autophagy-linked organelle remodeling in human external urethral sphincter myoblasts.Scientific reports · 2026Article
- Activation of mitophagy and proteasomal degradation confers resistance to developmental defects in postnatal skeletal muscle.Journal of biomedical science · 2025Article
- Mitophagy is required to protect against excessive skeletal muscle atrophy following hindlimb immobilization.Journal of biomedical science · 2025Article
- Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.International journal of molecular sciences · 2024Review
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Authors and funding
5 authors.
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Abstract
Skeletal muscle is a complex tissue comprising multinucleated and post-mitotic cells (i.e., myofibers). Given this, skeletal muscle must maintain a fine balance between growth and degradative signals. A major system regulating the remodeling of skeletal muscle is autophagy, where cellular quality control is mediated by the degradation of damaged cellular components. The accumulation of damaged cellular material can result in elevated apoptotic signaling, which is particularly relevant in skeletal muscle given its post-mitotic nature. Luckily, skeletal muscle possesses the unique ability to regenerate in response to injury. It is unknown whether a relationship between autophagy and apoptotic signaling exists in injured skeletal muscle and how autophagy deficiency influences myofiber apoptosis and regeneration. In the present study, we demonstrate that an initial inducible muscle-specific autophagy deficiency does not alter apoptotic signaling following cardiotoxin injury. This finding is presumably due to the re-establishment of ATG7 levels following injury, which may be attributed to the contribution of a functional
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