Caloric restriction and mitochondrial function in the ageing myocardium

Rohrbach, Susanne; Niemann, Bernd; Abushouk, Amir; Holtz, Juergen

doi:10.1016/j.exger.2006.02.001

Cited by 34 publications

(25 citation statements)

References 64 publications

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“…Moreover, and consistent with the notion that NRG regulates mitochondrial gene expression, the inhibition of ErbB2 causes mitochondrial dysfunction, thereby generating a marked decrease in oxidative capacity and the development of dilated cardiomyopathy (28,60). In this regard, it has been proposed that attenuation of NRG-ErbB signaling in cardiomyocytes is a causal factor for mitochondrial dysfunction and apoptotic cardiomyocyte loss in aging myocardium but also in failing myocardium (64). Chronic treatment with NRG, at picomolar concentrations, induces oxidative capacity by increasing mitochondrial biogenesis and the GLUT4 content in muscle cells (Fig.…”

Section: Is Neuregulin Involved In the Cellular Adaptations To Chronimentioning

confidence: 53%

Emerging role of neuregulin as a modulator of muscle metabolism

Gumà

Martínez-Redondo

López-Soldado

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Section: Is Neuregulin Involved In the Cellular Adaptations To Chronimentioning

confidence: 53%

Emerging role of neuregulin as a modulator of muscle metabolism

Gumà

Martínez-Redondo

López-Soldado

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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“…With aging, a decline in PGC-1a expression levels also occurs, with the latter being slowed by CR (8,100). Treatment with hexarelin or resveratrol rescues mitochondrial biogenesis and lipid metabolism by inducing a higher turnover of aged and damaged organelles (194). It should be mentioned that the changes in mitochondriogenesis are tissue specific, being more dramatic in the central nervous system (143), which is consistent with the generally higher susceptibility of neurons and other postmitotic cells to the aging process.…”

Section: E Decreased Mitochondrial Biogenesis In Aged Cellsmentioning

confidence: 63%

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

Terman

Kurz

Navrátil

et al. 2010

Antioxidants & Redox Signaling

427

375

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It is now generally accepted that aging and eventual death of multicellular organisms is to a large extent related to macromolecular damage by mitochondrially produced reactive oxygen species, mostly affecting long-lived postmitotic cells, such as neurons and cardiac myocytes. These cells are rarely or not at all replaced during life and can be as old as the whole organism. The inherent inability of autophagy and other cellular-degradation mechanisms to remove damaged structures completely results in the progressive accumulation of garbage, including cytosolic protein aggregates, defective mitochondria, and lipofuscin, an intralysosomal indigestible material. In this review, we stress the importance of crosstalk between mitochondria and lysosomes in aging. The slow accumulation of lipofuscin within lysosomes seems to depress autophagy, resulting in reduced turnover of effective mitochondria. The latter not only are functionally deficient but also produce increased amounts of reactive oxygen species, prompting lipofuscinogenesis. Moreover, defective and enlarged mitochondria are poorly autophagocytosed and constitute a growing population of badly functioning organelles that do not fuse and exchange their contents with normal mitochondria. The progress of these changes seems to result in enhanced oxidative stress, decreased ATP production, and collapse of the cellular catabolic machinery, which eventually is incompatible with survival. Antioxid. Redox Signal. 12, 503-535.

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“…A flood of recent work on DR in cardiac aging indicate that cardiac stem cells (294), mitochondrial function (124,230,275), and ROS production (60,209) have all been demonstrated to be beneficially affected by DR, and have all been implicated in the beneficial affects provided by restricting dietary intake.…”

Section: A Dietary Restrictionmentioning

confidence: 99%

Cardiac Aging: From Molecular Mechanisms to Significance in Human Health and Disease

Dai

Chen²,

Johnson³

et al. 2012

Antioxidants & Redox Signaling

278

223

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Cardiovascular diseases (CVDs) are the major causes of death in the western world. The incidence of cardiovascular disease as well as the rate of cardiovascular mortality and morbidity increase exponentially in the elderly population, suggesting that age per se is a major risk factor of CVDs. The physiologic changes of human cardiac aging mainly include left ventricular hypertrophy, diastolic dysfunction, valvular degeneration, increased cardiac fibrosis, increased prevalence of atrial fibrillation, and decreased maximal exercise capacity. Many of these changes are closely recapitulated in animal models commonly used in an aging study, including rodents, flies, and monkeys. The application of genetically modified aged mice has provided direct evidence of several critical molecular mechanisms involved in cardiac aging, such as mitochondrial oxidative stress, insulin/ insulin-like growth factor/PI3K pathway, adrenergic and renin angiotensin II signaling, and nutrient signaling pathways. This article also reviews the central role of mitochondrial oxidative stress in CVDs and the plausible mechanisms underlying the progression toward heart failure in the susceptible aging hearts. Finally, the understanding of the molecular mechanisms of cardiac aging may support the potential clinical application of several ''anti-aging'' strategies that treat CVDs and improve healthy cardiac aging.

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Caloric restriction and mitochondrial function in the ageing myocardium

Cited by 34 publications

References 64 publications

Emerging role of neuregulin as a modulator of muscle metabolism

Emerging role of neuregulin as a modulator of muscle metabolism

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

Cardiac Aging: From Molecular Mechanisms to Significance in Human Health and Disease

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