Authors
Kai Wang, Huimin Liu, Rong Chen, Qingtao Meng
Published in
Journal of anesthesia and translational medicine. Volume 5. Issue 4. Pages 206-212. Epub Sep 09, 2026.
Abstract
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.
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.
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.
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.
PMID:
42756859
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.
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