Cited by 263Mitochondrial Function and PathologyCardiac Fibrosis and RemodelingCardiovascular Function and Risk Factors

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

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Abel, E. D., Doenst, T.·2011·Cardiovascular Research

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.

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  1. [8]8. Naylor LH, George K, O'Driscoll G, Green DJ. The athlete's heart: a contemporary appraisal of the 'Morganroth hypothesis'. Sports Med 2008; 38 :69-90.

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Authors
Abel, E. D., & Doenst, T.
Affiliations
  • University of Utah (US)
  • Friedrich Schiller University Jena (DE)
Corresponding author
Abel, E. D.
Venue
Cardiovascular Research
Published
2011-01-21
Volume
90
Issue
2
Pages
234-242
ISSN
0008-6363 (ISSN-L)
OpenAlex
W2139425458
Cited by
263
References
109
Citations by year
2026: 11 · 2025: 9 · 2024: 8 · 2023: 12 · 2022: 11 · 2021: 14 · 2020: 18 · 2019: 15 · 2018: 19 · 2017: 20 · 2016: 16 · 2015: 24 · 2014: 31 · 2013: 26 · 2012: 22
FWCI
2.47
Type
journal article
Language
en
Open access
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (UO1 HL087947, U01HL087947)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK092065)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
cardiac hypertrophy, mitochondrial function, physiological hypertrophy, pathological hypertrophy, heart failure, mitochondrial proteome, mitochondrial bioenergetics, mitochondrial DNA, nuclear DNA, energy demand, pressure overload, fluid overload, contractile dysfunction
MeSH terms
Adaptation, Physiological, Animals, Heart, Cardiomegaly, Humans, Mitochondria, Myocardial Contraction, Signal Transduction

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