期刊
SCIENCE SIGNALING
卷 10, 期 490, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aal4161
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资金
- British Heart Foundation [PG/10/68/28528]
- King Saud bin Abdulaziz University for Health Sciences, Ministry of Higher Education for Saudi Arabia
- British Heart Foundation [PG/10/68/28528] Funding Source: researchfish
Diabetic stress increases the production of reactive oxygen species (ROS), leading to mitochondrial fragmentation and dysfunction. Wehypothesized that ROS-sensitive TRPM2 channels mediated diabetic stress-induced mitochondrial fragmentation. We found that chemical inhibitors, RNAi silencing, and genetic knockout of TRPM2 channels abolished the ability of high glucose to causemitochondrial fission in endothelial cells, a cell type that is particularly vulnerable to diabetic stress. Similar to high glucose, increasing ROS in endothelial cells by applying H2O2 induced mitochondrial fission. Ca2+ that entered through TRPM2 induced lysosomal membrane permeabilization, which led to the release of lysosomal Zn2+ and a subsequent increase in mitochondrial Zn2+. Zn2+ promoted the recruitment of the fission factor Drp-1 to mitochondria to trigger their fission. This signaling pathwaymay operate in aging-associated illnesses inwhich excessive mitochondrial fragmentation plays a central role.
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