“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 home...

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Bibliographic Details
Published inThe Journal of biological chemistry Vol. 293; no. 1; pp. 130 - 131
Main Author Wolf, Matthew J.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 05.01.2018
American Society for Biochemistry and Molecular Biology
Subjects
Calcium
Editors' Picks Highlights
eicosanoid biosynthesis
Heart Failure
Humans
Hydroxyeicosatetraenoic Acids
lipid
Mitochondria
Mitochondrial Membrane Transport Proteins
mitochondrial permeability transition (MPT)
Mitochondrial Permeability Transition Pore
phospholipase A
Phospholipases
mitochondrial permeability transition (MPT)
heart failure
phospholipase A
eicosanoid biosynthesis
lipid
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Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Commentary-1
Edited by George M. Carman
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.H117.001021