ArticlePLoS genetics2013
The NADPH metabolic network regulates human αB-crystallin cardiomyopathy and reductive stress in Drosophila melanogaster.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Sex differences inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Over-Intake of Plant-Derived Antioxidants, HInternational journal of molecular sciences · 2026Article
- Perturbation of NAD(P)H metabolism with theScience advances · 2026Article
- Reductive stress: The key pathway in metabolic disorders induced by overnutrition.Journal of advanced research · 2025Review
- Tissue-specific modulation of NADH consumption as an anti-aging intervention in Drosophila.bioRxiv : the preprint server for biology · 2025Article
- Age-regulated cycling metabolites are relevant for behavior.Aging cell · 2024Article
- Article
- Interplay between Nrf2 and αB-crystallin in the lens and heart of zebrafish under proteostatic stress.Frontiers in molecular biosciences · 2023Article
- Hepatoprotective Effect of Mitochondria-Targeted Antioxidant Mito-TEMPO against Lipopolysaccharide-Induced Liver Injury in Mouse.Mediators of inflammation · 2022Article
- Nampt Potentiates Antioxidant Defense in Diabetic Cardiomyopathy.Circulation research · 2021Article
- A role for actin flexibility in thin filament-mediated contractile regulation and myopathy.Nature communications · 2020Article
- Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy.Oxidative medicine and cellular longevity · 2020Review
- Centrosome Loss Triggers a Transcriptional Program To Counter Apoptosis-Induced Oxidative Stress.Genetics · 2019Article
- Epigenetics of Subcellular Structure Functioning in the Origin of Risk or Resilience to Comorbidity of Neuropsychiatric and Cardiometabolic Disorders.International journal of molecular sciences · 2018Review
- Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents.International journal of molecular sciences · 2017Review
- Distortion of the Actin A-Triad Results in Contractile Disinhibition and Cardiomyopathy.Cell reports · 2017Article
- Drosophila tools and assays for the study of human diseases.Disease models & mechanisms · 2016Review
- Review
- Getting folded: chaperone proteins in muscle development, maintenance and disease.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- Methods to assess Drosophila heart development, function and aging.Methods (San Diego, Calif.) · 2014Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Dominant mutations in the alpha-B crystallin (CryAB) gene are responsible for a number of inherited human disorders, including cardiomyopathy, skeletal muscle myopathy, and cataracts. The cellular mechanisms of disease pathology for these disorders are not well understood. Among recent advances is that the disease state can be linked to a disturbance in the oxidation/reduction environment of the cell. In a mouse model, cardiomyopathy caused by the dominant CryAB(R120G) missense mutation was suppressed by mutation of the gene that encodes glucose 6-phosphate dehydrogenase (G6PD), one of the cell's primary sources of reducing equivalents in the form of NADPH. Here, we report the development of a Drosophila model for cellular dysfunction caused by this CryAB mutation. With this model, we confirmed the link between G6PD and mutant CryAB pathology by finding that reduction of G6PD expression suppressed the phenotype while overexpression enhanced it. Moreover, we find that expression of mutant CryAB in the Drosophila heart impaired cardiac function and increased heart tube dimensions, similar to the effects produced in mice and humans, and that reduction of G6PD ameliorated these effects. Finally, to determine whether CryAB pathology responds generally to NADPH levels we tested mutants or RNAi-mediated knockdowns of phosphogluconate dehydrogenase (PGD), isocitrate dehydrogenase (IDH), and malic enzyme (MEN), the other major enzymatic sources of NADPH, and we found that all are capable of suppressing CryAB(R120G) pathology, confirming the link between NADP/H metabolism and CryAB.
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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.