CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway

Q: What are the key findings of this study?

SSO administration reduced myocardial injury and attenuated renal injury in diabetic rats subjected to myocardial ischemia-reperfusion.

Q: What is the clinical evidence from this study?

Population: Type 1 diabetes with myocardial ischemia-reperfusion injury (n=30). Intervention: Sulfo-N-succinimidyl oleate (SSO) vs. Diabetic ischemia-reperfusion without SSO. Primary outcome: Myocardial and renal injury markers (cTnI, CK-MB, Scr, BUN) (p=<0.05).

Q: What does this research mean for the field?

CD36 inhibition by SSO reduces myocardial injury and attenuates renal injury in diabetic rats subjected to myocardial ischemia-reperfusion. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To identify the role of the lipid transporter CD36 and the PI3K/Akt/eNOS pathway in myocardial ischemia-reperfusion-induced renal injury in diabetic rats.

Kai Wang; Huimin Liu; Rong Chen; Qingtao Meng

doi:10.1016/j.jatmed.2026.08.001

September 9, 2026Journal of Anesthesia and Translational MedicineOpen Access

CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway

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Key result

SSO reduces myocardial and renal injury after myocardial ischemia-reperfusion in diabetic rats.

P<0.05
n=30

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Why the study?

Whether the lipid transporter CD36 contributes to renal injury following myocardial ischemia-reperfusion in diabetes remains unknown.

Does CD36 inhibition with SSO reduce myocardial ischemia-reperfusion-induced renal injury in diabetic rats?

Key Points

To identify the role of the lipid transporter CD36 and the PI3K/Akt/eNOS pathway in myocardial ischemia-reperfusion-induced renal injury in diabetic rats.
Type 1 diabetic rats (n = 6 per group) received intravenous SSO, a pharmacological CD36 inhibitor, prior to undergoing myocardial ischemia-reperfusion (I/R) with or without ischemic postconditioning (IPostC).
Serum cardiac injury biomarkers (cTnI, CK-MB), renal function markers (BUN, Scr), lipid profiles (TG, FFA), and oxidative stress indices (SOD, MDA, 15-F2t-isoprostane) were quantified alongside echocardiographic functional parameters.
Renal tissue expression of CD36, phosphorylated Akt (p-Akt), and phosphorylated eNOS (p-eNOS) was measured via Western blotting.
Myocardial I/R significantly increased cardiac damage markers (cTnI, CK-MB), oxidative stress (MDA, 15-F2t-isoprostane), and renal dysfunction markers (BUN, Scr), while upregulating renal CD36, p-Akt, and p-eNOS expression (all P < 0.05 vs. diabetic sham).
SSO treatment significantly improved echocardiographic parameters (LVIDs, LVIDd, FS, LVEF), decreased myocardial injury and oxidative stress, and attenuated renal injury while lowering renal CD36, p-Akt, and p-eNOS levels (all P < 0.05 vs. diabetic I/R).
Ischemic postconditioning failed to confer significant cardioprotection or renoprotection and did not significantly alter oxidative stress or renal CD36, p-Akt, and p-eNOS expression in diabetic rats.

Structured PICO

Does CD36 inhibition with SSO reduce myocardial ischemia-reperfusion-induced renal injury in diabetic rats?

P

Population

30 male Sprague-Dawley rats with STZ-induced type 1 diabetes subjected to myocardial ischemia-reperfusion injury.

I

Intervention

Sulfo-N-succinimidyl oleate (SSO) 0.5 mg/kg intravenously 15 min before myocardial ischemia, or ischemic postconditioning (IPostC)

C

Comparator

Diabetic sham operation or diabetic ischemia-reperfusion without treatment

O

Outcome

Myocardial injury (cTnI, CK-MB) and renal function (Scr, BUN)surrogate

Main Result

p-value: p=<0.05

Inhibition of CD36 with SSO attenuates myocardial ischemia-reperfusion injury and secondarily reduces remote renal injury in diabetic rats.

Limitations

Model does not fully replicate all aspects of clinical cardiac surgery
Renoprotective effect of SSO may be largely indirect
Arterial blood gases were not monitored during the procedure
Detected only changes in protein expression without pathway-specific agonists or inhibitors

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Answers are grounded in this paper and cite their sources.

Implication

Does not support clinical use of SSO; leaves open whether CD36 inhibition benefits diabetic I/R patients.

Abstract

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.

Discussion

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Cite This Study

Wang et al. (2026) studied Type 1 diabetes with myocardial ischemia-reperfusion injury (n=30). Sulfo-N-succinimidyl oleate (SSO) vs. Diabetic ischemia-reperfusion without SSO was evaluated on Myocardial and renal injury markers (cTnI, CK-MB, Scr, BUN) (p=<0.05). SSO administration reduced myocardial injury and attenuated renal injury in diabetic rats subjected to myocardial ischemia-reperfusion.

synapsesocial.com/papers/6aa51e9d327956e4761f87c2 https://doi.org/10.1016/j.jatmed.2026.08.001

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CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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