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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2011 Dec 29;32(3):712–720. doi: 10.1161/ATVBAHA.111.227389

Figure 6. LG-Induced Endothelial Dysfunction: Role of Mitochondrial Superoxide Production and Prevention by AMPK Activation.

Figure 6

Acute LG exposure leads to rapid inhibition of eNOS and a reduction in bioavailable NO. This leads to a subsequent increase in mitochondrial ETC activity, mitochondrial membrane hyperpolarization, and increased mitochondrial superoxide production. Increased mitochondrial superoxide production can further reduce NO bioavailability and leads to increased cellular hydrogen peroxide levels that activate AMPK isoform α1 through a CaMKKβ dependent pathway. LG induced losses of NO bioavailability can be prevented/reversed by treatment with AMPKα2 activating agents acting through an LKB1 dependent activation pathway.