GNAS A-1121G Variant is Associated with Improved Diastolic Dysfunction in Response to Exercise Training in Heart Failure Patients

Alves, Alberto Jorge; Goldhammer, Ehud; Ribeiro, Fernando; Eynon, Nir; Cohen, Scott B.; Duarte, José Alberto; Viana, João L.; Sagiv, Michael; Oliveira, José

doi:10.1055/s-0032-1316365

Cited by 4 publications

(1 citation statement)

References 44 publications

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“…In addition, a sedentary lifestyle during healthy aging is associated with decreased left ventricular compliance, leading to diminished diastolic performance, while prolonged, sustained endurance training seems to preserve ventricular compliance with aging[73] and to enhance diastolic function in heart failure patients[74,75]. Moderate to vigorous physical activity may also offer protection against cardiac events by inducing short-term transient ischemia, conferring a window of protection against an ischemic insult of longer duration, a phenomenon known as cardiac preconditioning[76,77].…”

Section: Cardiovascular Protection Mechanisms Induced By Physical Actmentioning

confidence: 99%

Physical activity in primary and secondary prevention of cardiovascular disease: Overview updated

Alves¹,

Viana²,

Cavalcante³

et al. 2016

WJC

162

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Although the observed progress in the cardiovascular disease treatment, the incidence of new and recurrent coronary artery disease remains elevated and constitutes the leading cause of death in the developed countries. Three-quarters of deaths due to cardiovascular diseases could be prevented with adequate changes in lifestyle, including increased daily physical activity. New evidence confirms that there is an inverse dose-response relationship between physical activity and cardiovascular disease and mortality risk. However, participation in moderate to vigorous physical activity may not fully attenuate the independent effect of sedentary activities on increased risk for cardiovascular diseases. Physical activity also plays an important role in secondary prevention of cardiovascular diseases by reducing the impact of the disease, slowing its progress and preventing recurrence. Nonetheless, most of eligible cardiovascular patients still do not benefit from secondary prevention/cardiac rehabilitation programs. The present review draws attention to the importance of physical activity in the primary and secondary prevention of cardiovascular diseases. It also addresses the mechanisms by which physical activity and regular exercise can improve cardiovascular health and reduce the burden of the disease.

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Section: Cardiovascular Protection Mechanisms Induced By Physical Actmentioning

confidence: 99%

Physical activity in primary and secondary prevention of cardiovascular disease: Overview updated

Alves¹,

Viana²,

Cavalcante³

et al. 2016

WJC

162

View full text Add to dashboard Cite

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Genetic variants associated with exercise performance in both moderately trained and highly trained individuals

et al. 2020

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Adaptation to exercise training is a complex trait that may be influenced by genetic variants. We identified 36 single nucleotide polymorphisms (SNPs) that had been previously associated with endurance or strength performance, exercise-related phenotypes or exercise intolerant disorders. A MassARRAY multiplex genotyping assay was designed to identify associations with these SNPs against collected endurance fitness phenotype parameters obtained from 2 exercise cohorts (Gene SMART study; n=58 and Hawaiian Ironman Triathlon 2008; n=115). These parameters included peak power output (PP), a time trial (TT), lactate threshold (LT), maximal oxygen uptake (VO2 max) in recreationally active individuals and a triathlon time to completion (Hawaiian Ironman Triathlon cohort only). A nominal significance threshold of α<0.05 was used to identify 17 variants (11 in the Gene SMART population and 6 in the Hawaiian Ironman Triathlon cohort) which were significantly associated with performance gains in highly trained individuals. The variant rs1474347 located in Interleukin 6 (IL6) was the only variant with a false discovery rate < 0.05 and was found to be associated with gains in VO2 max (additional 4.016 mL/(kg•min) for each G allele inherited) after training in the Gene SMART cohort. In summary, this study found further evidence to suggest that genetic variance can influence training response in a moderately trained cohort and provides an example of the potential application of genomic research in the assessment of exercise trait response.

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Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis

Guarnieri

Anthony

Gozdiff

et al. 2021

American Journal of Physiology-Heart and Circulatory Physiology

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Adipose tissue homeostasis plays a central role in cardiovascular physiology, and the presence of thermogenically active brown adipose tissue (BAT) has recently been associated with cardiometabolic health. We have previously shown that adipose tissue-specific deletion of HuR (Adipo-HuR-/-) reduces BAT-mediated adaptive thermogenesis, and the goal of this work was to identify the cardiovascular impacts of Adipo-HuR-/-. We found that Adipo-HuR-/- mice exhibit a hypercontractile phenotype that is accompanied by increased left ventricle wall thickness and hypertrophic gene expression. Furthermore, hearts from Adipo-HuR-/- display increased fibrosis via picrosirius red staining and periostin expression. To identify underlying mechanisms, we applied both RNA-seq and weighted gene co-expression network analysis (WGCNA) across both cardiac and adipose tissue to define HuR-dependent changes in gene expression as well as significant relationships between adipose tissue gene expression and cardiac fibrosis. RNA-seq results demonstrated a significant increase in pro-inflammatory gene expression in both cardiac and subcutaneous white adipose tissue (scWAT) from Adipo-HuR-/- mice that is accompanied by an increase in serum levels of both TNF-ᵯC; and IL-6. In addition to inflammation-related genes, WGCNA identified a significant enrichment in extracellular vesicle-mediated transport and exosome-associated genes in scWAT whose expression most significantly associated with degree of cardiac fibrosis observed in Adipo-HuR-/- mice, implicating these processes as a likely adipose-to-cardiac paracrine mechanism. These results are significant in that they demonstrate the spontaneous onset of cardiovascular pathology in an adipose tissue-specific gene deletion model and contribute to our understanding of how disruptions in adipose tissue homeostasis may mediate cardiovascular disease.

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GNAS A-1121G Variant is Associated with Improved Diastolic Dysfunction in Response to Exercise Training in Heart Failure Patients

Cited by 4 publications

References 44 publications

Physical activity in primary and secondary prevention of cardiovascular disease: Overview updated

Physical activity in primary and secondary prevention of cardiovascular disease: Overview updated

Genetic variants associated with exercise performance in both moderately trained and highly trained individuals

Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis

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