Based on recent advances on the Ca²⁺-activated F₁F_O-ATPase features, a novel multistep mechanism involving the mitochondrial F₁F_O complex in the formation and opening of the still enigmatic mitochondrial permeability transition pore (MPTP), is proposed. MPTP opening makes the inner mitochondrial membrane (IMM) permeable to ions and solutes and, through cascade events, addresses cell fate to death. Since MPTP forms when matrix Ca²⁺ concentration rises and ATP is hydrolyzed by the F₁F_O-ATPase, conformational changes, triggered by Ca²⁺ insertion in F₁, may be transmitted to F_O and locally modify the IMM curvature. These events would cause F₁F_O-ATPase dimer dissociation and MPTP opening.

基于Ca ²⁺激活的F ₁ F _O -ATPase特性的最新进展，提出了一种新的多步机理，涉及线粒体F ₁ F _O络合物在仍然神秘的线粒体通透性过渡孔（MPTP）的形成和开放中。 。MPTP的开放使线粒体内膜（IMM）可以渗透离子和溶质，并通过级联事件解决细胞命运直至死亡。由于当基质Ca ²⁺浓度升高并且ATP被F ₁ F _O -ATPase水解时会形成MPTP ，因此由Ca ²⁺插入F ₁触发的构象变化可能会传递给F_O并局部修改IMM曲率。这些事件将导致F ₁ F _O -ATPase二聚体解离和MPTP开放。