ArticleExperimental and therapeutic medicine2020
Homocysteine induces mitochondrial dysfunction and oxidative stress in myocardial ischemia/reperfusion injury through stimulating ROS production and the ERK1/2 signaling pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Pooled it
- Effects of Vitamin B6 and Folic Acid on Cardiometabolic Biomarkers and Cardiac Oxidative Stress in Homocysteine-Loaded Rats.Biomedicines · 2026Article
- The complex link of the folate-homocysteine axis to myocardial hypertrophy and heart failure: from mechanistic exploration to clinical vision.Journal of advanced research · 2026Review
- B vitamins and cardiovascular health: mechanisms, clinical evidence, and precision prevention strategies.Nutrition & metabolism · 2026Review
- Propolis alleviates brain tissue damage and oxidative abnormalities in streptozotocin (STZ)-induced diabetes.Journal, genetic engineering & biotechnology · 2026Article
- Seminal Homocysteine Levels in Men With Asthenozoospermia: Correlation With Sperm Parameters and Vitamin BTheScientificWorldJournal · 2026Article
- The relationship between homocysteine and new-onset atrial fibrillation in patients with acute myocardial infarction.Annals of medicine · 2025Article
- Genotype Combinations and Genetic Risk Score Analyses ofCurrent issues in molecular biology · 2025Article
- Nicotinamide N-Methyltransferase in Cardiovascular Diseases: Metabolic Regulator and Emerging Therapeutic Target.Biomolecules · 2025Review
- AIMP3 maintains cardiac homeostasis by regulating the editing activity of methionyl-tRNA synthetase.Nature cardiovascular research · 2025Article
- Cytokine profiles and metabolic dysregulation in endometriosis: insights into diagnostic and therapeutic targets.Molecular biology reports · 2025Article
- Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Article
- [MiR-224-5p overexpression inhibits oxidative stress by regulating the PI3K/Akt/FoxO1 axis to attenuate hypoxia/reoxygenation-induced cardiomyocyte injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Nicotinamide N-Methyltransferase (NNMT): A New Hope for Treating Aging and Age-Related Conditions.Metabolites · 2024Review
- Article
- Article
- Pretreatment with geniposide mitigates myocardial ischemia/reperfusion injury by modulating inflammatory response through TLR4/NF-κB pathway.European journal of histochemistry : EJH · 2023Article
- Evaluation of serum vitamin B12 levels in patients with COVID-19 infection: A case-control study.Journal of medical biochemistry · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute oxidative stress and mitochondrial dysfunction are crucial for acute myocardial ischemia-reperfusion (AMI/R) injury, which may induce cell or mitochondrial membrane rupture and myocardial infarction. Plasma homocysteine (Hcy) expression levels are positively associated with risk of cardiovascular disease, and ERK1/2 exert anti-apoptotic and cardioprotective effects on AMI/R injury. However, the precise molecular mechanism of action underlying the effects of Hcy and the ERK1/2 signaling pathway on mitochondrial dysfunction and oxidative stress in AMI/R injury remains unclear. In the present study, AMI/R injury models were established in an animal model treated with Hcy and in H9C2 cells that were treated with hypoxia-reoxygenation. Mitochondrial function and oxidative stress were evaluated. The results demonstrated that Hcy enhanced ERK1/2 protein expression levels and oxidative stress, induced cytochrome c translocation and mitochondria dysfunction, and caused cardiac dysfunction in rats with AMI/R injury. However, an ERK1/2 inhibitor effectively protected AMI/R injury rats from Hcy-induced cardiac dysfunction and oxidative stress. In conclusion, Hcy induced mitochondrial dysfunction and oxidative stress in AMI/R injury through stimulating ROS production and the ERK1/2 signaling pathway. An ERK1/2 inhibitor may be an effective new therapeutic method for treating Hcy-induced cardiac dysfunction in patients with AMI/R injury.
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Registered trials
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