Research ArticleCell Biology

High glucose–induced ROS activates TRPM2 to trigger lysosomal membrane permeabilization and Zn2+-mediated mitochondrial fission

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Sci. Signal.  01 Aug 2017:
Vol. 10, Issue 490, eaal4161
DOI: 10.1126/scisignal.aal4161

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Fragmented by diabetic stress

The high circulating glucose concentrations characteristic of diabetes induce the excessive production of reactive oxygen species (ROS), which triggers mitochondrial fragmentation. The cation channel TRPM2 is activated by ROS, leading Abuarab et al. to investigate the role of this channel in mitochondrial fragmentation in endothelial cells, which become dysfunctional in diabetics. In response to high glucose–induced oxidative stress, Ca2+ influx through TRPM2 channels caused lysosomal permeabilization and redistribution of lysosomal Zn2+ to mitochondria. The increase in mitochondrial Zn2+ led to the recruitment of the fission factor Drp-1, resulting in mitochondrial fragmentation. This pathway may play a role in the pathology of aging-associated diseases that are characterized by increased mitochondrial fragmentation.