Cardiolipin remodeling in Barth syndrome and other hereditary cardiomyopathies.


Journal

Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730

Informations de publication

Date de publication:
01 08 2020
Historique:
received: 17 10 2019
revised: 19 12 2019
accepted: 13 04 2020
pubmed: 30 4 2020
medline: 5 1 2021
entrez: 30 4 2020
Statut: ppublish

Résumé

Mitochondria play a prominent role in cardiac energy metabolism, and their function is critically dependent on the integrity of mitochondrial membranes. Disorders characterized by mitochondrial dysfunction are commonly associated with cardiac disease. The mitochondrial phospholipid cardiolipin directly interacts with a number of essential protein complexes in the mitochondrial membranes including the respiratory chain, mitochondrial metabolite carriers, and proteins critical for mitochondrial morphology. Barth syndrome is an X-linked disorder caused by an inherited defect in the biogenesis of the mitochondrial phospholipid cardiolipin. How cardiolipin deficiency impacts on mitochondrial function and how mitochondrial dysfunction causes cardiomyopathy has been intensively studied in cellular and animal models of Barth syndrome. These findings may also have implications for the molecular mechanisms underlying other inherited disorders associated with defects in cardiolipin, such as Sengers syndrome and dilated cardiomyopathy with ataxia (DCMA).

Identifiants

pubmed: 32348916
pii: S0925-4439(20)30148-4
doi: 10.1016/j.bbadis.2020.165803
pii:
doi:

Substances chimiques

Cardiolipins 0
Mitochondrial Proteins 0
Phosphatidic Acids 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

165803

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Edoardo Bertero (E)

Comprehensive Heart Failure Center (CHFC), University Clinic Würzburg, 97078 Würzburg, Germany.

Ilona Kutschka (I)

Comprehensive Heart Failure Center (CHFC), University Clinic Würzburg, 97078 Würzburg, Germany.

Christoph Maack (C)

Comprehensive Heart Failure Center (CHFC), University Clinic Würzburg, 97078 Würzburg, Germany.

Jan Dudek (J)

Comprehensive Heart Failure Center (CHFC), University Clinic Würzburg, 97078 Würzburg, Germany. Electronic address: Dudek_J@ukw.de.

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Classifications MeSH