ArticleMolecular genetics and metabolism2017
Excess coenzyme A reduces skeletal muscle performance and strength in mice overexpressing human PANK2.
Article in Molecular genetics and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Proteomics- and Metabolomics-Based Investigation of the Effects ofAnimals : an open access journal from MDPI · 2026Article
- A liquid chromatography-mass spectrometry method to quantify total Coenzyme A concentration and isotopic labeling.bioRxiv : the preprint server for biology · 2026Article
- Diagnosis and Treatment of Pantothenate Kinase-Associated Neurodegeneration (PKAN): A Systematic Review.Cureus · 2023Review
- The epigenetic regulatory effect of histone acetylation and deacetylation on skeletal muscle metabolism-a review.Frontiers in physiology · 2023Review
- Generation and Validation of an Anti-Human PANK3 Mouse Monoclonal Antibody.Biomolecules · 2022Article
- Pantothenate kinase activation relieves coenzyme A sequestration and improves mitochondrial function in mice with propionic acidemia.Science translational medicine · 2021Article
- [Research advances in the pathogenesis and treatment of neurodegeneration with brain iron accumulation].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Article
- The Pathophysiological Role of CoA.International journal of molecular sciences · 2020Review
- Metabolomic analysis of primary human skeletal muscle cells during myogenic progression.Scientific reports · 2020Article
- A therapeutic approach to pantothenate kinase associated neurodegeneration.Nature communications · 2018Article
- Nudt19 is a renal CoA diphosphohydrolase with biochemical and regulatory properties that are distinct from the hepatic Nudt7 isoform.The Journal of biological chemistry · 2018Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Coenzyme A (CoA) is a cofactor that is central to energy metabolism and CoA synthesis is controlled by the enzyme pantothenate kinase (PanK). A transgenic mouse strain expressing human PANK2 was derived to determine the physiological impact of PANK overexpression and elevated CoA levels. The Tg(PANK2) mice expressed high levels of the transgene in skeletal muscle and heart; however, CoA was substantially elevated only in skeletal muscle, possibly associated with the comparatively low endogenous levels of acetyl-CoA, a potent feedback inhibitor of PANK2. Tg(PANK2) mice were smaller, had less skeletal muscle mass and displayed significantly impaired exercise tolerance and grip strength. Skeletal myofibers were characterized by centralized nuclei and aberrant mitochondria. Both the content of fully assembled complex I of the electron transport chain and ATP levels were reduced, while markers of oxidative stress were elevated in Tg(PANK2) skeletal muscle. These abnormalities were not detected in the Tg(PANK2) heart muscle, with the exception of spotty loss of cristae organization in the mitochondria. The data demonstrate that excessively high CoA may be detrimental to skeletal muscle function.
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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.