ArticleJournal of molecular and cellular cardiology2012
Homocysteine induces cardiomyocyte dysfunction and apoptosis through p38 MAPK-mediated increase in oxidant stress.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 89 citations in OpenAlex.
- Associations of methyl donor and methylation inhibitor levels during anti-oxidant therapy in heart failure.Journal of physiology and biochemistry · 2021Trial
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Effects of Vitamin B6 and Folic Acid on Cardiometabolic Biomarkers and Cardiac Oxidative Stress in Homocysteine-Loaded Rats.Biomedicines · 2026Article
- One-carbon metabolism and cardiovascular disease: Molecular mechanisms, genetic influences, and epigenetic regulation.Biochemistry and biophysics reports · 2026Review
- Study on the evaluation of left atrial structure and function in patients with H-type hypertension using 4D automated left atrial quantitative.BMC cardiovascular disorders · 2026Article
- AIMP3 maintains cardiac homeostasis by regulating the editing activity of methionyl-tRNA synthetase.Nature cardiovascular research · 2025Article
- Myocardial mitochondrial antiviral signaling protein promotes heart Ischemia-reperfusion injury via RIG-I signaling in mice.Nature communications · 2025Article
- Hyperhomocysteinemia-Induced Alterations in Protein Expression and Oxidative Stress Parameters in Rat Heart.Physiological research · 2024Article
- Integrated metabolomics and proteomics reveal biomarkers associated with hemodialysis in end-stage kidney disease.Frontiers in pharmacology · 2023Article
- Induction of apoptosis and autosis in cardiomyocytes by the combination of homocysteine and copper via NOX-mediated p62 expression.Cell death discovery · 2022Article
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- Effect of methionine feeding on oxidative stress, intracellular calcium and contractility in cardiomyocytes isolated from male and female rats.Molecular and cellular biochemistry · 2021Article
- Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways.Cellular and molecular life sciences : CMLS · 2021Review
- The Importance of Telomere Shortening for Atherosclerosis and Mortality.Journal of cardiovascular development and disease · 2020Review
- Effect of Methionine Diet on Time-Related Metabolic and Histopathological Changes of Rat Hippocampus in the Model of Global Brain Ischemia.Biomolecules · 2020Article
- Calcium Export from Neurons and Multi-Kinase Signaling Cascades Contribute to Ouabain Neuroprotection in Hyperhomocysteinemia.Biomolecules · 2020Article
- Scutellarin-treated exosomes increase claudin 5, occludin and ZO1 expression in rat brain microvascular endothelial cells.Experimental and therapeutic medicine · 2019Article
- Article
- Effects of procyanidin on cardiomyocyte apoptosis after myocardial ischemia reperfusion in rats.BMC cardiovascular disorders · 2018Article
- SYKT Alleviates Doxorubicin-Induced Cardiotoxicity via Modulating ROS-Mediated p53 and MAPK Signal Pathways.Evidence-based complementary and alternative medicine : eCAM · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Elevated plasma homocysteine (Hcy) is a risk factor for cardiovascular disease. While Hcy has been shown to promote endothelial dysfunction by decreasing the bioavailability of nitric oxide and increasing oxidative stress in the vasculature, the effects of Hcy on cardiomyocytes remain less understood. In this study we explored the effects of hyperhomocysteinemia (HHcy) on myocardial function ex vivo and examined the direct effects of Hcy on cardiomyocyte function and survival in vitro. Studies with isolated hearts from wild type and HHcy mice (heterozygous cystathionine-beta synthase deficient mice) demonstrated that HHcy mouse hearts had more severely impaired cardiac relaxation and contractile function and increased cell death following ischemia reperfusion (I/R). In isolated cultured adult rat ventricular myocytes, exposure to Hcy for 24 h impaired cardiomyocyte contractility in a concentration-dependent manner, and promoted apoptosis as revealed by terminal dUTP nick-end labeling and cleaved caspase-3 immunoblotting. These effects were associated with activation of p38 MAPK, decreased expression of thioredoxin (TRX) protein, and increased production of reactive oxygen species (ROS). Inhibition of p38 MAPK by the selective inhibitor SB203580 (5 μM) prevented all of these Hcy-induced changes. Furthermore, adenovirus-mediated overexpression of TRX in cardiomyocytes significantly attenuated Hcy-induced ROS generation, apoptosis, and impairment of myocyte contractility. Thus, Hcy may increase the risk for CVD not only by causing endothelial dysfunction, but also by directly exerting detrimental effects on cardiomyocytes.
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