Mitochondrial fission/fusion and cardiomyopathy

Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for ‘primary mitochondrial cardiac diseases’ may be because such an ent...

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Bibliographic Details
Published inCurrent opinion in genetics & development Vol. 38; pp. 38 - 44
Main Author GW, Dorn
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2016
Subjects
Animals
Cardiomyopathies - genetics
Cardiomyopathies - metabolism
Cardiomyopathies - pathology
Humans
Medical Education
Mice
Mitochondria - genetics
Mitochondrial Dynamics - genetics
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
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Summary:Mitochondria are highly abundant in and essential to the beat-to-beat contractile performance of hearts. However, relatively few cardiac diseases have been attributed to primary mitochondrial dysfunction. The paucity of evidence for ‘primary mitochondrial cardiac diseases’ may be because such an entity does not exist. Alternately, the consequences of mitochondrial dysfunction on hearts may be so severe that long-term viability is severely impaired and affected individuals are therefore not included in standard genetic screens of adult heart disease subjects. Here, I review accumulating experimental evidence that impairing mitochondrial fission or fusion causes cardiomyopathy in otherwise normal mice, and consider how these data could motivate screening of perinatal cardiomyopathy subjects for damaging mutations of mitochondrial fission and fusion factors.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ObjectType-Review-3
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ISSN:0959-437X
1879-0380
1879-0380
DOI:10.1016/j.gde.2016.03.001