Our the latest scientific studies suggest that this is due to defective trafficking of late endosomes to lysosomes, with concomitant homotypic fusion with the afflicted vesicular compartments [5]. The defect in lysosome-directed trafficking also influences autophagic flux, with resultant accumulation of autophagosomes [five]. Finally, the integrity of the cell membrane https://h2dcfda14578.topbloghub.com/32243893/triptolide-no-further-a-mystery