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. 2022 Mar 24;118(17):3305–3319. doi: 10.1093/cvr/cvac030

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© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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The MAM represents a unique compartment enabling NOX4-localized ROS signalling and ER-mitochondrial calcium communication. Serum starvation or ischaemia–reperfusion (IR) injury can lead to mitochondrial calcium overload and cell death but an increase in NOX4 levels at the MAM prevents excessive calcium transfer between the ER and mitochondria, thereby inhibiting opening of the mitochondrial permeability transition pore and cell death. Mechanistically, NOX4 results in the enhancement of MAM-located Akt activity via a redox inhibition of the phosphatase PP2a. Akt in turn is able to phosphorylate ER InsP3R channels which decrease the release of calcium from the ER to the mitochondria.