Fig. 4: Effect of CD36 knockdown on fatty acid uptake and mitochondrial function in human CMs.

a, Quantitative PCR showing CD36 mRNA expression in hiPSC-CMs transfected with siRNA targeting CD36 versus scrambled control siRNA, presented as relative fold change. **P < 0.01 (Mann–Whitney test; each dot represents an experimental replicate). b, Long-chain fatty acid uptake after 1-h incubation with BODIPY FL C16 in scrambled and CD36-siRNA-treated hiPSC-CMs. Data are shown as mean ± s.e.m.; n = 10 per group. ****P < 0.0001 (Mann–Whitney test). c, Averaged real-time OCR in hiPSC-CMs following CD36 knockdown or transfection with scrambled control, measured using seahorse extracellular flux analysis. After 1 h of starvation, cells were provided Pal as the sole substrate, followed by sequential treatments with Eto (β-oxidation inhibitor), Oligo (ATP synthase inhibitor), CCCP (respiratory uncoupler) and R/A (respiratory chain inhibitors). d, β-oxidation rate, calculated as OCR reduction following etomoxir treatment. Data are shown as mean ± s.e.m.; scrambled n = 11, CD36 siRNA n = 8. ****P < 0.0001 (Mann–Whitney test); dots represent experimental replicates. e, Comparison of averaged mitochondrial function using seahorse extracellular flux analyzer. f, Maximal respiratory capacity, defined as the difference between OCR following CCCP and rotenone/antimycin treatment in hiPSC-CMs treated with CD36 siRNA or scrambled control. Data are presented as mean ± s.e.m.; scrambled n = 9, CD36 siRNA n = 14. ***P < 0.0001 (Mann–Whitney test); dots represent experimental replicates. Pal, palmitate; Eto, etomoxir; Oligo, oligomycin; R/A, rotenone/antimycin.