ArticleCell2007
Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice.
Article in Cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 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.
The trial behind it
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
249 citing papers in PubMed, 426 citations in OpenAlex.
- Associations of methyl donor and methylation inhibitor levels during anti-oxidant therapy in heart failure.Journal of physiology and biochemistry · 2021Trial
- Trial
- Mitophagy Facilitates Cytosolic Proteostasis to Preserve Cardiac Function.Circulation research · 2026Article
- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- The R120G knock-in mutation in αB-crystallin is insufficient to induce cardiomyopathy in mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Reductive Stress and Ferroptosis: Linking Insulin Signaling to Metabolic Dysfunction.Biomolecules · 2026Review
- Over-Intake of Plant-Derived Antioxidants, HInternational journal of molecular sciences · 2026Article
- Clinical Studies Using Intranasal Therapies for Parkinson's Disease: A Review.Advanced pharmaceutical bulletin · 2026Review
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- NRF2-Targeted Therapy in Cardiovascular Disease Transitions from Systemic Activation to Precision Redox Medicine.Antioxidants (Basel, Switzerland) · 2026Review
- Dynamic regulation of receptor-modulated endothelial NADPH oxidases.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Perturbation of NAD(P)H metabolism with theScience advances · 2026Article
- A Micro-Engineered Heart Tissue Model of Desmin-related Cardiomyopathy Caused by Mutant αB Crystallin.bioRxiv : the preprint server for biology · 2025Article
- Reductive stress: The key pathway in metabolic disorders induced by overnutrition.Journal of advanced research · 2025Review
- Antioxidants in Cardiovascular Health: Implications for Disease Modeling Using Cardiac Organoids.Antioxidants (Basel, Switzerland) · 2025Review
- Dynamic regulation of the oxidative stress response by the E3 ligase TRIP12.Cell reports · 2025Article
- Nanomedicine-Driven Modulation of Reductive Stress for Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Oxygen needs sulfur, sulfur needs oxygen: a relationship of interdependence.The EMBO journal · 2025Review
- Adolescent Stress-Induced Ventral Hippocampus Redox Dysregulation Underlies Behavioral Deficits and Excitatory/Inhibitory Imbalance Related to Schizophrenia.Schizophrenia bulletin · 2025Article
- Tissue-specific modulation of NADH consumption as an anti-aging intervention in Drosophila.bioRxiv : the preprint server for biology · 2025Article
189 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
The autosomal dominant mutation in the human alphaB-crystallin gene inducing a R120G amino acid exchange causes a multisystem, protein aggregation disease including cardiomyopathy. The pathogenesis of cardiomyopathy in this mutant (hR120GCryAB) is poorly understood. Here, we show that transgenic mice overexpressing cardiac-specific hR120GCryAB recapitulate the cardiomyopathy in humans and find that the mice are under reductive stress. The myopathic hearts show an increased recycling of oxidized glutathione (GSSG) to reduced glutathione (GSH), which is due to the augmented expression and enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase, and glutathione peroxidase. The intercross of hR120GCryAB cardiomyopathic animals with mice with reduced G6PD levels rescues the progeny from cardiac hypertrophy and protein aggregation. These findings demonstrate that dysregulation of G6PD activity is necessary and sufficient for maladaptive reductive stress and suggest a novel therapeutic target for abrogating R120GCryAB cardiomyopathy and heart failure in humans.
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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.