ArticlePloS one2023
CHAC1 inactivation is effective to preserve muscle glutathione but is insufficient to protect against muscle wasting in cachexia.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Scientific landscape of oxidative stress in sarcopenia: from bibliometric analysis to hotspots review.Frontiers in medicine · 2024Pooled it
- Silymarin alleviates cisplatin-induced cachexia via modulating tripartite motif containing 63 (TRIM63) and myogenin.Indian journal of pharmacology · 2026Article
- Article
- Article
- Protein S-glutathionylation confers cellular resistance to ferroptosis induced by glutathione depletion.Redox biology · 2025Article
- Screening of hub genes for sepsis-induced myopathy by weighted gene co-expression network analysis and protein-protein interaction network construction.BMC musculoskeletal disorders · 2024Article
- Oxidative Metabolism as a Cause of Lipid Peroxidation in the Execution of Ferroptosis.International journal of molecular sciences · 2024Review
- Transcriptome analysis revealed differences in gene expression in sheep muscle tissue at different developmental stages.BMC genomic data · 2024Article
- Article
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- Review
- Carnosol ameliorated cancer cachexia-associated myotube atrophy by targeting P5CS and its downstream pathways.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscle wasting is one of the main characteristics of cachexia associated with cancer and other chronic diseases and is often exacerbated by antineoplastic agents. Increased oxidative stress is associated with muscle wasting, along with depletion of glutathione, the most abundant endogenous antioxidant. Therefore, boosting endogenous glutathione has been proposed as a therapeutic strategy to prevent muscle wasting. Here, we tested this hypothesis by inactivating CHAC1, an intracellular glutathione degradation enzyme. We found CHAC1 expression is increased under multiple muscle wasting conditions in animal models, including fasting, cancer cachexia, and chemotherapy. The elevation of muscle Chac1 expression is associated with reduced glutathione level. CHAC1 inhibition via CRSPR/Cas9 mediated knock-in of an enzyme inactivating mutation demonstrates a novel strategy to preserve muscle glutathione levels under wasting conditions but fails to prevent muscle wasting in mice. These results suggest that preserving intracellular glutathione level alone may not be sufficient to prevent cancer or chemotherapy induced muscle wasting.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.