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Heart failure-induced activation of phospholipase iPLA₂γ generates hydroxyeicosatetraenoic acids opening the mitochondrial permeability transition pore.

ABSTRACT: Congestive heart failure typically arises from cardiac myocyte necrosis/apoptosis, associated with the pathological opening of the mitochondrial permeability transition pore (mPTP). mPTP opening decreases the mitochondrial membrane potential leading to the activation of Ca²⁺-independent phospholipase A₂γ (iPLA₂γ) and the production of downstream toxic metabolites. However, the array of enzymatic mediators and the exact chemical mechanisms responsible for modulating myocardial mPTP opening remain unclear. Herein, we demonstrate that human heart failure activates specific myocardial mitochondrial phospholipases that increase Ca²⁺-dependent production of toxic hydroxyeicosatetraenoic acids (HETEs) and attenuate the activity of phospholipases that pr

SUBMITTER: Moon SH

PROVIDER: S-EPMC5766913 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Heart failure-induced activation of phospholipase iPLA₂γ generates hydroxyeicosatetraenoic acids opening the mitochondrial permeability transition pore.

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Dataset Information

Heart failure-induced activation of phospholipase iPLA2γ generates hydroxyeicosatetraenoic acids opening the mitochondrial permeability transition pore.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Heart failure-induced activation of phospholipase iPLA₂γ generates hydroxyeicosatetraenoic acids opening the mitochondrial permeability transition pore.