ArticleProceedings of the National Academy of Sciences of the United States of America2024
Zfp697 is an RNA-binding protein that regulates skeletal muscle inflammation and remodeling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Gait analysis for functional evaluation in a surgical hindlimb suspension model of muscle atrophy.The Journal of physiology · 2026Article
- Decoding Human Placental Cellular and Molecular Responses to Obesity and Fetal Growth.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Article
- Advanced lung cancer inflammation index is associated with mortality in critically ill patients with non-traumatic cerebral hemorrhage.Scientific reports · 2025Article
- Zfp697 is an RNA-binding protein that regulates skeletal muscle inflammation and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle ImplicatesbioRxiv : the preprint server for biology · 2024Article
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21 authors.
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Abstract
Skeletal muscle atrophy is a morbidity and mortality risk factor that happens with disuse, chronic disease, and aging. The tissue remodeling that happens during recovery from atrophy or injury involves changes in different cell types such as muscle fibers, and satellite and immune cells. Here, we show that the previously uncharacterized gene and protein Zfp697 is a damage-induced regulator of muscle remodeling. Zfp697/ZNF697 expression is transiently elevated during recovery from muscle atrophy or injury in mice and humans. Sustained Zfp697 expression in mouse muscle leads to a gene expression signature of chemokine secretion, immune cell recruitment, and extracellular matrix remodeling. Notably, although Zfp697 is expressed in several cell types in skeletal muscle, myofiber-specific Zfp697 genetic ablation in mice is sufficient to hinder the inflammatory and regenerative response to muscle injury, compromising functional recovery. We show that Zfp697 is an essential mediator of the interferon gamma response in muscle cells and that it functions primarily as an RNA-interacting protein, with a very high number of miRNA targets. This work identifies Zfp697 as an integrator of cell-cell communication necessary for tissue remodeling and regeneration.
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