ArticleOxidative medicine and cellular longevity2020
Metabolomic Analysis of the Ameliorative Effect of Enhanced Proline Metabolism on Hypoxia-Induced Injury in Cardiomyocytes.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 20 citations in OpenAlex.
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- Nitidine Chloride Alleviates Hypoxic Stress via PINK1-Parkin-Mediated Mitophagy in the Mammary Epithelial Cells of Milk Buffalo.Animals : an open access journal from MDPI · 2024Article
- Proline metabolic reprogramming modulates cardiac remodeling induced by pressure overload in the heart.Science advances · 2024Article
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- Protective effect and mechanism of procyanidin B2 against hypoxic injury of cardiomyocytes.Heliyon · 2023Article
- Transcriptome analysis reveals ADAMTS15 is a potential inflammation-related gene in remote ischemic postconditioning.Frontiers in cardiovascular medicine · 2023Article
- Metabolomic and transcriptomic studies of improvements in myocardial infarction due to Pycr1 deletion.Journal of cellular and molecular medicine · 2023Article
- Cardioprotective Mechanism of Leonurine against Myocardial Ischemia through a Liver-Cardiac Crosstalk Metabolomics Study.Biomolecules · 2022Article
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- Redox Regulation and Oxidative Stress in Mammalian Oocytes and Embryos DevelopedInternational journal of environmental research and public health · 2021Review
- Protective Effect of Optic Atrophy 1 on Cardiomyocyte Oxidative Stress: Roles of Mitophagy, Mitochondrial Fission, and MAPK/ERK Signaling.Oxidative medicine and cellular longevity · 2021Article
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10 authors at 1 institution in 1 country.
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Abstract
backgroundCoronary heart disease is currently the leading cause of death in humans. Its poor prognosis and high mortality are associated with myocardial ischemia, which leads to metabolic disorder-related cardiomyocyte apoptosis and reactive oxygen species (ROS) production. Previous cardiovascular metabolomics studies in humans and mice have shown that proline metabolism is severely altered after cardiomyocyte hypoxia. Proline dehydrogenase (PRODH) is located on the inner mitochondrial membrane and is an enzyme that catalyzes the first step of proline catabolism, which plays an important role in improving the cellular redox state. In vitro oxygen-glucose deprivation can mimic in vivo myocardial ischemic injury. This study is aimed at investigating whether enhancing proline metabolism by overexpressing PRODH can ameliorate hypoxia-induced injury in cardiomyocytes and to reveal the related altered metabolites and mechanistic pathway via untargeted metabolomics analysis. METHODS AND
resultsFirst, through public database analysis and RT-qPCR and western blot analyses in a cardiomyocyte hypoxia model, we found that the expression of the proline-degrading enzyme PRODH was downregulated after myocardial infarction and hypoxia exposure. Second, LDH assays, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), DHE staining, flow cytometric apoptosis analysis with DCFH and Annexin V-FITC/PI, and western blot analysis were used to assess the injury level in cardiomyocytes. Enhanced proline metabolism induced by PRODH overexpression reduced the levels of reactive oxidative stress and apoptosis, whereas PRODH knockdown had the opposite effects. Third, untargeted metabolomics analysis revealed that the protective effect was associated with significant changes in metabolism linked to sphingolipid signaling pathways, unsaturated fatty acid biosynthesis, phosphocreatine, glutathione disulfide, aminoacyl-tRNA biosynthesis, and ABC transporters.
conclusionsOur study demonstrated a protective effect of enhanced proline metabolism in cardiomyocytes under hypoxia, providing a novel strategy for exploring new treatments for coronary heart disease.
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