ArticleAnatolian journal of cardiology2019
The cystathionine γ-lyase/hydrogen sulfide pathway mediates the trimetazidine-induced protection of H9c2 cells against hypoxia/reoxygenation-induced apoptosis and oxidative stress.
Article in Anatolian journal of cardiology, 2019. 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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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Multifunctional microneedle patch loaded with microfluidic-synthesized hybrid gas-nanozyme for myocardial infarction treatment.Journal of nanobiotechnology · 2025Article
- Review
- Curcumin reduces myocardial ischemia-reperfusion injury, by increasing endogenous HMolecular biology reports · 2024Article
- Characterization of the mFrontiers in immunology · 2024Article
- Regulatory effects of trimetazidine in cardiac ischemia/reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Metabolic regulation to treat bipolar depression: mechanisms and targeting by trimetazidine.Molecular psychiatry · 2023Review
- Coronary "Microvascular Dysfunction": Evolving Understanding of Pathophysiology, Clinical Implications, and Potential Therapeutics.International journal of molecular sciences · 2023Review
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Trimetazidine enhances myocardial angiogenesis in pressure overload-induced cardiac hypertrophy mice through directly activating Akt and promoting the binding of HSF1 to VEGF-A promoter.Acta pharmacologica Sinica · 2022Article
- NLRP3 inflammasome activation in gestational diabetes mellitus placentas is associated with hydrogen sulfide synthetase deficiency.Experimental and therapeutic medicine · 2022Article
- The Potential of Hydrogen Sulfide Donors in Treating Cardiovascular Diseases.International journal of molecular sciences · 2021Review
- Trimetazidine in Heart Failure.Frontiers in pharmacology · 2020Review
- Advances in the Protective Mechanism of NO, HFrontiers in cardiovascular medicine · 2020Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTrimetazidine is a piperazine-derived metabolic agent. It exerts cardioprotective effects against myocardial ischemia/reperfusion (I/R) injury. In addition, studies confirm that the cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway serves a beneficent role in attenuating myocardial I/R injury. However, the underlying role of the CSE/H2S pathway in the trimetazidine-induced protection against myocardial I/R injury remains elusive. Therefore, this study investigated whether trimetazidine ameliorates hypoxia/reoxygenation (H/R)-induced H9c2 cardiomyocyte injuries in an in vitro cell model of myocardial I/R injury, by enhancing the CSE/H2S pathway.
methodsThe H9c2 cell viability was determined with a cell counting Kit-8.
resultsTrimetazidine significantly increased the cell viability and decreased lactate dehydrogenase (LDH) release in H/R-treated H9c2 cells. Additionally, trimetazidine increased the H2S levels and the CSE mRNA and protein levels, promoting the CSE/H2S pathway under H/R conditions. The inhibition of the CSE/H2S pathway, induced by transfection with specific siRNA against human CSE (si-CSE), eliminated the trimetazidine-induced upregulation of cell viability, downregulation of LDH release, increase of caspase-3 activity and apoptosis regulator BAX expression, and the decrease of apoptosis regulator Bcl-2 expression, which suggests involvement of the CSE/H2S pathway in trimetazidine-induced cardioprotection. Furthermore, trimetazidine mitigated the H/R-induced increase in reactive oxygen species production and NADPH oxidase 2 expression, and decrease in superoxide dismutase activity and glutathione level, in H9c2 cells. These effects were also reversed by si-CSE.
conclusionThis study revealed that the CSE/H2S pathway mediates the trimetazidine-induced protection of H9c2 cardiomyocytes against H/R-induced damage by inhibiting apoptosis and oxidative stress.
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