ArticleNature communications2022
Mechanism of action and therapeutic route for a muscular dystrophy caused by a genetic defect in lipid metabolism.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
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- A Computational Approach to Identify Novel Protein Targets Uncovers New Potential Mechanisms of Action of Mirtazapine S(+) and R(-) Enantiomers in Rett Syndrome.Journal of neurochemistry · 2025Article
- PNPLA6 regulates retinal homeostasis by choline through phospholipid turnover.Nature communications · 2025Article
- Scientific and Technological Prospecting on Polymeric Particles Containing Extracellular Matrix Peptides for the Treatment of Duchenne Muscular Dystrophy.Recent advances in drug delivery and formulation · 2025Review
- Defects in integrin complex formation promoteLife science alliance · 2024Article
- CHKB-DT: A Long Noncoding RNA Critical for Cardiovascular Health.Circulation research · 2024Article
- Metabolic Flexibility of the Heart: The Role of Fatty Acid Metabolism in Health, Heart Failure, and Cardiometabolic Diseases.International journal of molecular sciences · 2024Review
- Article
- A rare homozygous variant ofFrontiers in cardiovascular medicine · 2024Article
- Molecular subtypes of ALS are associated with differences in patient prognosis.Nature communications · 2023Article
- Integrative Metabolomics and Proteomics Detected Hepatotoxicity in Mice Associated with Alkaloids fromToxins · 2022Article
- Megaconial congenital muscular dystrophy due to novel CHKB variants: a case report and literature review.Skeletal muscle · 2022Review
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
Abstract
CHKB encodes one of two mammalian choline kinase enzymes that catalyze the first step in the synthesis of the membrane phospholipid phosphatidylcholine. In humans and mice, inactivation of the CHKB gene (Chkb in mice) causes a recessive rostral-to-caudal muscular dystrophy. Using Chkb knockout mice, we reveal that at no stage of the disease is phosphatidylcholine level significantly altered. We observe that in affected muscle a temporal change in lipid metabolism occurs with an initial inability to utilize fatty acids for energy via mitochondrial β-oxidation resulting in shunting of fatty acids into triacyglycerol as the disease progresses. There is a decrease in peroxisome proliferator-activated receptors and target gene expression specific to Chkb
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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.