Structural basis for a complex I mutation that blocks pathological ROS production

Reactive oxygen species (ROS) production by reverse electron transfer (RET) through complex I is thought to cause tissue damage from heart attacks. Here, the authors combine in vivo work with biochemical and cryo-EM analyses to characterize the effects of a P25L mutation in the ND6 subunit of mitoch...

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Autores principales: Zhan Yin, Nils Burger, Duvaraka Kula-Alwar, Dunja Aksentijević, Hannah R. Bridges, Hiran A. Prag, Daniel N. Grba, Carlo Viscomi, Andrew M. James, Amin Mottahedin, Thomas Krieg, Michael P. Murphy, Judy Hirst
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/1317dd8d29fd49259db11814845c32ea
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Sumario:Reactive oxygen species (ROS) production by reverse electron transfer (RET) through complex I is thought to cause tissue damage from heart attacks. Here, the authors combine in vivo work with biochemical and cryo-EM analyses to characterize the effects of a P25L mutation in the ND6 subunit of mitochondrial complex I. They observe that this mutation does not affect oxidative phosphorylation but renders complex I unable to generate ROS by RET: ND6-P25L mice are protected against cardiac ischaemia–reperfusion injury, thus providing evidence for the proposed role of ROS production in myocardial infarction.