ArticleExperimental and therapeutic medicine2017
Mechanism of myocardial ischemia/reperfusion-induced acute kidney injury through DJ-1/Nrf2 pathway in diabetic rats.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- PCSK9 and Other Metabolic Targets to Counteract Ischemia/Reperfusion Injury in Acute Myocardial Infarction and Visceral Vascular Surgery.Journal of clinical medicine · 2022Review
- Article
- Mechanism of circadian regulation of the NRF2/ARE pathway in renal ischemia-reperfusion.Experimental and therapeutic medicine · 2021Article
- PARK7 Protects Against Chronic Kidney Injury and Renal Fibrosis by Inducing SOD2 to Reduce Oxidative Stress.Frontiers in immunology · 2021Article
- Protective role of DJ-1 in endotoxin-induced acute kidney injury.American journal of physiology. Renal physiology · 2020Article
- ND-13, a DJ-1-Derived Peptide, Attenuates the Renal Expression of Fibrotic and Inflammatory Markers Associated with Unilateral Ureter Obstruction.International journal of molecular sciences · 2020Article
- Article
- Tetramethylpyrazine exerts a protective effect against injury from acute myocardial ischemia by regulating the PI3K/Akt/GSK-3β signaling pathway.Cellular & molecular biology letters · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of the present study was to investigate acute kidney injury (AKI) induced by myocardial ischemia/reperfusion (MIR) in diabetic rats and elucidate its underlying mechanism. A rat model of MIR was established by left anterior descending coronary artery occlusion for 30 min, followed by reperfusion for 2 h. Rats were randomly divided into four groups: i) Sham group, ii) sham + MIR group, iii) diabetic group and iv) diabetes + MIR group. Myocardial injury was detected by plasma creatine kinase isoenzyme MB and lactate dehydrogenase assays. AKI induced by MIR in diabetic rats was characterized by increases in cystatin C and β2-microglobulin levels. Oxidative stress injury was accompanied by an increase of malondialdehyde levels and a decrease of total antioxidative capacity in the renal tissues. Immunohistochemistry and western blot analysis demonstrated that the expression of DJ-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) were significantly increased in the diabetes + MIR group compared with that in the sham + MIR and diabetic groups. Taken together, these results suggested that AKI induced by MIR in diabetic rats may be associated with activation of the DJ-1/Nrf2 pathway.
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