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. 2021 May 21;12(6):523. doi: 10.1038/s41419-021-03813-6

Fig. 5. Inhibition of CD36 enhances mitochondrial fatty acid oxidation and ameliorates the metabolism reprogramming induced by HG.

Fig. 5

A−C FA-driven oxygen consumption rate (PA-dependent OCR) curve (A) and OCR, ECAR (B, C) quantified data from HK-2 cells under NG, HG, and HG + kCD36 conditions. D The levels of p-AMPK, p-ACC, and CPT1 were analyzed by western blot. NG: 5.6 mM d-glucose; M: NG + 24.4 mM mannitol; HG: 30 mM d-glucose; HG + C: HG + LV3 empty vector (LV3-NC); HG + kCD36: HG + CD36 mutant vector (LV3-shRNA); NG + kCD36: NG + CD36 mutant vector (LV3-shRNA). Data are expressed as the mean ± SD of four independent experiments. **P < 0.01 versus the NG group; #P < 0.05, compared with the HG group by ANOVA.