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Publication
Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy.
Authors
Abel ED, Doenst T
Submitted By
E. Dale Abel on 3/4/2015
Status
Published
Journal
Cardiovascular research
Year
2011
Date Published
5/1/2011
Volume : Pages
90 : 234 - 242
PubMed Reference
Abstract
Cardiac hypertrophy is a stereotypic response of the heart to increased
workload. The nature of the workload increase may vary depending on the stimulus
(repetitive, chronic, pressure, or volume overload). If the heart fully adapts
to the new loading condition, the hypertrophic response is considered
physiological. If the hypertrophic response is associated with the ultimate
development of contractile dysfunction and heart failure, the response is
considered pathological. Although divergent signalling mechanisms may lead to
these distinct patterns of hypertrophy, there is some overlap. Given the close
relationship between workload and energy demand, any form of cardiac hypertrophy
will impact the energy generation by mitochondria, which are the key organelles
for cellular ATP production. Significant changes in the expression of nuclear
and mitochondrially encoded transcripts that impact mitochondrial function as
well as altered mitochondrial proteome composition and mitochondrial energetics
have been described in various forms of cardiac hypertrophy. Here, we review
mitochondrial alterations in pathological and physiological hypertrophy. We
suggest that mitochondrial adaptations to pathological and physiological
hypertrophy are distinct, and we shall review potential mechanisms that might
account for these differences.
Investigators with authorship
Name
Institution
E. Dale Abel
University of Iowa
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(看片视频) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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