"HETE"ing up mitochondria in human heart failure.

A decade of research has established the phospholipase iPLA2γ as being involved in cardiomyocyte dysfunction and necrosis leading to heart failure, but the mechanisms by which iPLA2γ acts and its interaction with the mitochondrial permeability transition pore (mPTP) that is critical for cardiac homeostasis are unclear. New investigations by Moon et al. demonstrate that mitochondria in failing hearts undergo dynamic shifts in PLA2 isoform expression, leading to a redistribution of eicosanoid composition that contributes to pathologic mPTP opening.