Distinct mPTP activation mechanisms in ischaemia–reperfusion: contributions of Ca2+, ROS, pH, and inorganic polyphosphate

Abstract

Transient Ca(2+)/polyP-mediated mPTP opening during ischaemia may serve to protect cells against cytosolic Ca(2+) overload, whereas ROS/pH-mediated sustained mPTP opening on reperfusion induces cell death.