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Regulatory effects of trimetazidine in cardiac ischemia/reperfusion injury

Ischemia/reperfusion (I/R) injury is a tissue damage during reperfusion after an ischemic condition. I/R injury is induced by pathological cases including stroke, myocardial infarction, circulatory arrest, sickle cell disease, acute kidney injury, trauma, and sleep apnea. It can lead to increased morbidity and mortality in the context of these processes. Mitochondrial dysfunction is one of the hallmarks of I/R insult, which is induced via reactive oxygen species (ROS) production, apoptosis, and autophagy. MicroRNAs (miRNAs, miRs) are non-coding RNAs that play a main regulatory role in gene expression. Recently, there are evidence, which miRNAs are the major modulators of cardiovascular diseases, especially myocardial I/R injury. Cardiovascular miRNAs, specifically miR-21, and probably miR-24 and miR-126 have protective effects on myocardial I/R injury. Trimetazidine (TMZ) is a new class of metabolic agents with an anti-ischemic activity. It has beneficial effects on chronic stable angina by suppressing mitochondrial permeability transition pore (mPTP) opening. The present review study addressed the different mechanistic effects of TMZ on cardiac I/R injury. Online databases including Scopus, PubMed, Web of Science, and Cochrane library were assessed for published studies between 1986 and 2021. TMZ, an antioxidant and metabolic agent, prevents the cardiac reperfusion injury by regulating AMP-activated protein kinase (AMPK), cystathionine-γ-lyase enzyme (CSE)/hydrogen sulfide (H2S), and miR-21. Therefore, TMZ protects the heart against I/R injury by inducing key regulators such as AMPK, CSE/H2S, and miR-21.

 

Comments：

It is interesting to note that miRNAs, specifically miR-21, miR-24, and miR-126, may have protective effects on myocardial I/R injury. These miRNAs may regulate gene expression to help prevent mitochondrial dysfunction induced by ROS production, apoptosis, and autophagy.

Additionally, TMZ, as an antioxidant and metabolic agent, may also prevent cardiac reperfusion injury by regulating AMP-activated protein kinase (AMPK), cystathionine-γ-lyase enzyme (CSE)/hydrogen sulfide (H2S), and miR-21. By inducing these key regulators, TMZ may protect the heart against I/R injury.

It is important to note that this review study assessed published studies between 1986 and 2021, so new research may provide additional insights into the mechanisms of action and potential therapeutic applications of miRNAs and TMZ in the context of I/R injury.

Related Products

Cat.No. Product Name Information
S4543 Trimetazidine dihydrochloride Trimetazidine dihydrochloride (Yoshimilon, Kyurinett, Vastarel F) is a kind of drug for treatment of chronic ischemic disorders. It improves myocardial glucose utilization through inhibition of fatty acid metabolism, known as fatty acid oxidation inhibitor.

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