Impaired mitochondrial biogenesis is a common feature to myocardial hypertrophy and end-stage ischemic heart failure

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
Annalinda PisanoCarla Giordano

Abstract

Mitochondrial (mt) DNA depletion and oxidative mtDNA damage have been implicated in the process of pathological cardiac remodeling. Whether these features are present in the early phase of maladaptive cardiac remodeling, that is, during compensated cardiac hypertrophy, is still unknown. We compared the morphologic and molecular features of mt biogenesis and markers of oxidative stress in human heart from adult subjects with compensated hypertrophic cardiomyopathy and heart failure. We have shown that mtDNA depletion is a constant feature of both conditions. A quantitative loss of mtDNA content was associated with significant down-regulation of selected modulators of mt biogenesis and decreased expression of proteins involved in mtDNA maintenance. Interestingly, mtDNA depletion characterized also the end-stage phase of cardiomyopathies due to a primary mtDNA defect. Oxidative stress damage was detected only in failing myocardium.

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Citations

Jan 28, 2017·American Journal of Respiratory Cell and Molecular Biology·Kara N GossMarlowe W Eldridge
Mar 2, 2018·Antioxidants & Redox Signaling·Paul J M WijnkerJolanda van der Velden
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Methods Mentioned

BETA
laser capture microdissection
transmission electron microscopy
Reverse Transcription
Polymerase Chain Reaction
Assay
protein assay
electrophoresis

Software Mentioned

ImageJ
oxyblot
Graphpad InStat

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