Mitochondrial function and structure in experimental canine congestive heart failure

Walker, Joanne G.; Bishop, Sanford P.

doi:10.1093/cvr/5.4.444

Cited by 9 publications

(3 citation statements)

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“…66 In contrast, no changes in mitochondrial morphology were noted in a dog model of right ventricular hypertrophy and congestive heart failure. 67 Disorganization of mitochondrial cristae combined with a reduction in cristae density has been reported for failing rat hearts after aortic constriction. 11 This study also revealed significant remodelling of the mitochondrial proteome, characterized by reduced content of the majority of FAO proteins and .50% of the electron transport chain subunits that were detected.…”

Section: Mitochondrial Morphology and Function After The Onset Of LV ...mentioning

confidence: 94%

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

Abel

Doenst

2011

Cardiovascular Research

229

190

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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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Section: Mitochondrial Morphology and Function After The Onset Of LV ...mentioning

confidence: 94%

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

Abel

Doenst

2011

Cardiovascular Research

229

190

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“…Decreased mitochondrial phos phorylation efficiency and oxidation rates are seen in some models [49][50][51], while in others no changes are noted [52][53][54], It is probable that the degree of change is dependent on the degree of damage. A final common pathway for many types of cardiac disease is the accu mulation of large amounts of calcium in mi tochondria, but the mechanisms of this accu mulation are unknown.…”

Section: Cardiac Failurementioning

confidence: 98%

Myocardial Calcium Regulation in Disease

Jacobson¹,

Ambudkar

Shamoo

1983

Pathol Immunopathol Res

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“…The results of many studies regarding the respiratory activity of isolated mitochondria have varied from depressed function, normal function, and increased function in stable hypertrophy, and either normal or depressed function in hypertrophy with failure. The varying results due to different animal models and isolation techniques have been reviewed by several authors [ 320 , 321 , 322 ]. Rosca and Hoppel [ 321 ] have reviewed the effects of various forms of pathology on mitochondria.…”

Section: Mitochondriamentioning

confidence: 99%

Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts

Bishop

Zhang

2022

Biology

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The cardiomyocyte undergoes dramatic changes in structure, metabolism, and function from the early fetal stage of hyperplastic cell growth, through birth and the conversion to hypertrophic cell growth, continuing to the adult stage and responding to various forms of stress on the myocardium, often leading to myocardial failure. The fetal cell with incompletely formed sarcomeres and other cellular and extracellular components is actively undergoing mitosis, organelle dispersion, and formation of daughter cells. In the first few days of neonatal life, the heart is able to repair fully from injury, but not after conversion to hypertrophic growth. Structural and metabolic changes occur following conversion to hypertrophic growth which forms a barrier to further cardiomyocyte division, though interstitial components continue dividing to keep pace with cardiac growth. Both intra- and extracellular structural changes occur in the stressed myocardium which together with hemodynamic alterations lead to metabolic and functional alterations of myocardial failure. This review probes some of the questions regarding conditions that regulate normal and pathologic growth of the heart.

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Mitochondrial function and structure in experimental canine congestive heart failure

Cited by 9 publications

References 0 publications

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy

Myocardial Calcium Regulation in Disease

Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts

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