ArticleCell reports2018
Defective Mitochondrial Cardiolipin Remodeling Dampens HIF-1α Expression in Hypoxia.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- Cardiolipin preserves TNature metabolism · 2026Article
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- The role of HIF-1α in myocardial ischemia protection mechanisms and multi-target rational regulation strategies for natural products.Frontiers in pharmacology · 2026Review
- Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Imaging flow cytometry-based cellular screening elucidates pathophysiology in individuals with Variants of Uncertain Significance.Genome medicine · 2025Article
- ANP Increases ZnCurrent medical science · 2025Article
- Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome.Basic research in cardiology · 2023Article
- Molecular mechanisms of AMPK/YAP/NLRP3 signaling pathway affecting the occurrence and development of ankylosing spondylitis.Journal of orthopaedic surgery and research · 2023Article
- Metabolic switch from fatty acid oxidation to glycolysis in knock-in mouse model of Barth syndrome.EMBO molecular medicine · 2023Article
- The Complex Relationship between Hypoxia Signaling, Mitochondrial Dysfunction and Inflammation in Calcific Aortic Valve Disease: Insights from the Molecular Mechanisms to Therapeutic Approaches.International journal of molecular sciences · 2023Review
- The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection.Frontiers in pharmacology · 2023Review
- Potent anti-inflammatory responses: Role of hydrogen in IL-1α dominated early phase systemic inflammation.Frontiers in pharmacology · 2023Article
- Pharmacological mechanisms of sodium-glucose co-transporter 2 inhibitors in heart failure with preserved ejection fraction.BMC cardiovascular disorders · 2022Article
- HIF-1α-regulated lncRNA-TUG1 promotes mitochondrial dysfunction and pyroptosis by directly binding to FUS in myocardial infarction.Cell death discovery · 2022Article
- An antioxidant system through conjugating superoxide dismutase onto metal-organic framework for cardiac repair.Bioactive materials · 2022Article
- Review
- Review
- Lipidome Atlas of the Developing Heart Uncovers Dynamic Membrane Lipid Attributes Underlying Cardiac Structural and Metabolic Maturation.Research (Washington, D.C.) · 2022Article
- Re-Expression of Tafazzin Isoforms in TAZ-Deficient C6 Glioma Cells Restores Cardiolipin Composition but Not Proliferation Rate and Alterations in Gene Expression.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs, integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin remodeling, upon loss of the cardiolipin acyl transferase tafazzin, decreases HIF-1α signaling in hypoxia. Tafazzin deficiency does not affect posttranslational HIF-1α regulation but rather HIF-1α gene expression, a dysfunction recapitulated in iPSC-derived cardiomyocytes from Barth syndrome patients with tafazzin deficiency. RNA-seq analyses confirmed drastically altered signaling in tafazzin mutant cells. In hypoxia, tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-κB activation and concomitantly HIF-1α gene expression. Tafazzin-deficient mice hearts display reduced HIF-1α levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondrial cardiolipin remodeling dampens HIF-1α signaling due to a lack of NF-κB activation through reduced mitochondrial ROS production, decreasing HIF-1α transcription.
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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.