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Updated: Sep 19, 2026
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied
Kai Wang1, Huimin Liu1, Rong Chen1
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430000, China.
Background:
CD36, a lipid transporter, is markedly upregulated in the diabetic kidney. However, whether CD36 contributes to renal injury following myocardial ischemia-reperfusion (I/R) in diabetes remains unknown. This study aimed to identify the role of CD36 in myocardial I/R-induced renal injury in diabetic rats and to investigate the mechanisms involved.
Methods:
Type 1 diabetic rats received intravenous SSO, a CD36 inhibitor, and were then subjected to myocardial ischemia-reperfusion (I/R) with ischemic postconditioning. Cardiac and renal function, tissue injury markers, and oxidative stress were assessed using commercial assay kits. Protein expression was analyzed by Western blotting.
Results:
After myocardial I/R, oxidative stress increased and renal function deteriorated. CD36 and the PI3K/Akt/eNOS pathway were upregulated in the kidney, potentially reflecting a compensatory protective response. SSO, a CD36 inhibitor, reduced myocardial injury, lowered renal CD36 and p-Akt/p-eNOS expression, and attenuated renal injury, indicating that its renoprotective effect was largely secondary to cardioprotection. In contrast, ischemic postconditioning conferred little protection in diabetic rats.
Conclusions:
These findings indicate that CD36 is upregulated in the kidney after myocardial I/R in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway as a compensatory response. CD36 inhibition by SSO reduced myocardial injury and, in turn, attenuated renal injury, suggesting that CD36 is associated with myocardial I/R-induced renal injury.
