PPARGC1A and Platelet storage pool disease: We observed a higher percentage of fibroblasts from sPD patients treated with AntiOxCIN4 in the S-phase of cell cycle, as well as a decrease in mtDNA copy number and protein content of PGC1-α, a master regulator of mitochondrial biogenesis, suggesting that cells are trying to repair mitochondrial abnormalities most likely avoiding the accumulation of defective mtDNA and mitochondria-defective cells.