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These findings corroborate with a previous functional study conducted by Sharma and colleagues [50], who demonstrated that PPAR silencing in endothelial cells leads to profound mitochondrial dysfunction by accentuating transmembrane depolarization and ROS production, lowering the cellular ATP levels and hampering the eNOS/Hsp90 axis, critical for energy metabolism regulation

References 1.Ambrosy A

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These theoretical effects could be shown in a practical trial by Ahmed et al

In sensitivity analysis, we also included an isoform of l-carnitine, acetyl-carnitine, proxied by three genetic variants reaching genome-wide significance from the same GWAS as l-carnitine [20]