Genetic manipulation of cardiac ageing

Cannon, Leah; Bodmer, Rolf

doi:10.1113/jp270563

Cited by 8 publications

(6 citation statements)

References 56 publications

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“…Again, the functional consequences for healthspan are not clear for reasons similar to those articulated in describing the aging worm intestine. For a tissue-specific decline in organ function with age, the fly has one clear homologue of human organ aging: it has a beating heart with many features in common with the mammalian heart and has been used to investigate invertebrate cardiac aging in a number of studies 14 . Remarkably, there have even been reports describing the benefits of exercise on the aging fly heart 67 , 80 , and this is an exciting research area which needs to be more broadly studied.…”

Section: Other Healthspan Metrics In Invertebrate Modelsmentioning

confidence: 99%

Geroscience approaches to increase healthspan and slow aging

Melov

2016

F1000Res

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For decades, researchers in the biology of aging have focused on defining mechanisms that modulate aging by primarily studying a single metric, sometimes described as the “gold standard” lifespan. Increasingly, geroscience research is turning towards defining functional domains of aging such as the cardiovascular system, skeletal integrity, and metabolic health as being a more direct route to understand why tissues decline in function with age. Each model used in aging research has strengths and weaknesses, yet we know surprisingly little about how critical tissues decline in health with increasing age. Here I discuss popular model systems used in geroscience research and their utility as possible tools in preclinical studies in aging.

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Section: Other Healthspan Metrics In Invertebrate Modelsmentioning

confidence: 99%

Geroscience approaches to increase healthspan and slow aging

Melov

2016

F1000Res

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“…Both fly and human hearts experience age-related morphological and functional decline. Several genes in mammals that regulate oxidative stress and cardiac hypertrophy also affect the cardiac aging in a fruit fly [7]. Elderly rhesus monkeys exhibit degenerative calcifications of the aortic and mitral valves, myocardial hypertrophy, lipofuscin accumulation, interstitial fibrosis, myocardial infarction, and congestive heart failure [4].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Quan

Xin

Tian

et al. 2020

Oxidative Medicine and Cellular Longevity

132

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Mitochondrial DNA (mtDNA) damage is associated with the development of cardiovascular diseases. Cardiac aging plays a central role in cardiovascular diseases. There is accumulating evidence linking cardiac aging to mtDNA damage, including mtDNA mutation and decreased mtDNA copy number. Current wisdom indicates that mtDNA is susceptible to damage by mitochondrial reactive oxygen species (mtROS). This review presents the cellular and molecular mechanisms of cardiac aging, including autophagy, chronic inflammation, mtROS, and mtDNA damage, and the effects of mitochondrial biogenesis and oxidative stress on mtDNA. The importance of nucleoid-associated proteins (Pol γ), nuclear respiratory factors (NRF1 and NRF2), the cGAS-STING pathway, and the mitochondrial biogenesis pathway concerning the development of mtDNA damage during cardiac aging is discussed. Thus, the repair of damaged mtDNA provides a potential clinical target for preventing cardiac aging.

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“…Aging flies exhibit altered heart metabolism with increased arrhythmia, myofibrillar disorganization and dysregulation of Insulin and TOR pathways. Strikingly, reducing Insulin or TOR pathway activation increases lifespan and delays cardiac aging [ 151 , 152 , 153 ], showing that aging can be controlled by nutrient-sensing (reviewed elsewhere [ 154 ]).…”

Section: Pathological Mechanisms Investigatedmentioning

confidence: 99%

Drosophila in the Heart of Understanding Cardiac Diseases: Modeling Channelopathies and Cardiomyopathies in the Fruitfly

Taghli-Lamallem

Plantie

Jagla

2016

JCDD

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Cardiovascular diseases and, among them, channelopathies and cardiomyopathies are a major cause of death worldwide. The molecular and genetic defects underlying these cardiac disorders are complex, leading to a large range of structural and functional heart phenotypes. Identification of molecular and functional mechanisms disrupted by mutations causing channelopathies and cardiomyopathies is essential to understanding the link between an altered gene and clinical phenotype. The development of animal models has been proven to be efficient for functional studies in channelopathies and cardiomyopathies. In particular, the Drosophila model has been largely applied for deciphering the molecular and cellular pathways affected in these inherited cardiac disorders and for identifying their genetic modifiers. Here we review the utility and the main contributions of the fruitfly models for the better understanding of channelopathies and cardiomyopathies. We also discuss the investigated pathological mechanisms and the discoveries of evolutionarily conserved pathways which reinforce the value of Drosophila in modeling human cardiac diseases.

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Genetic manipulation of cardiac ageing

Cited by 8 publications

References 56 publications

Geroscience approaches to increase healthspan and slow aging

Geroscience approaches to increase healthspan and slow aging

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Drosophila in the Heart of Understanding Cardiac Diseases: Modeling Channelopathies and Cardiomyopathies in the Fruitfly

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