Homocysteine induces mitochondrial dysfunction and oxidative stress in myocardial ischemia/reperfusion injury through stimulating ROS production and the ERK1/2 signaling pathway
- Lei Wang
- Heping Niu
- Jun Zhang
Affiliations: Department of Cardiology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China
- Published online on: May 12, 2020 https://doi.org/10.3892/etm.2020.8735
Copyright: © Wang
et al. This is an open access article distributed under the
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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.