Alcohol consumption and heart failure: A systematic review

Djoussé, Luc; Gaziano, J. Michael

doi:10.1007/s11883-008-0017-z

Cited by 117 publications

(82 citation statements)

References 48 publications

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“…A number of theories have been put forward for the onset and development of alcoholic complications, including oxidative damage, deposition of triglycerides, altered fatty acid extraction, decreased myofilament Ca 2+ sensitivity, impaired protein metabolism, and mitochondrial anomalies [193][194][195][196][197][198][199] . Not surprisingly, oxidative stress and mitochondrial damage have been shown to contribute to the toxic effects of alcoholic liver and myocardial injuries [200][201][202] .…”

Section: Alcohol Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

Mitochondria and Oxidative Stress in the Cardiorenal Metabolic Syndrome

et al. 2012

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Mitochondria play a fundamental role in the maintenance of normal structure, function, and survival of tissues. There is considerable evidence for mitochondrial dysfunction in association with metabolic diseases including insulin resistance, obesity, diabetes, and the cardiorenal metabolic syndrome. The phenomenon of reactive oxygen species (ROS)-induced ROS release through interactions between cytosolic and mitochondrial oxidative stress contributes to a vicious cycle of enhanced oxidative stress and mitochondrial dysfunction. Activation of the cytosolic and mitochondrial NADPH oxidase system, impairment of the mitochondrial electron transport, activation of p66shc pathway-targeting mitochondria, endoplasmic reticular stress, and activation of the mammalian target of the rapamycin-S6 kinase pathway underlie dysregulation of mitochondrial dynamics and promote mitochondrial oxidative stress. These processes are further modulated by acetyltransferases including sirtuin 1 and sirtuin 3, the former regulating nuclear acetylation and the latter regulating mitochondrial acetylation. The regulation of mitochondrial functions by microRNAs forms an additional layer of molecular control of mitochondrial oxidative stress. Alcohol further exacerbates mitochondrial oxidative stress induced by overnutrition and promotes the development of metabolic diseases.

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Section: Alcohol Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

Mitochondria and Oxidative Stress in the Cardiorenal Metabolic Syndrome

et al. 2012

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“…Moderate alcohol consumption is associated with hypertension [47] and higher doses result in an increased risk of MI and stroke [48,49]. According to Saremi and Arora, [50] there is an increased risk of hypertriglyceridemia, cardiomyopathy, hypertension, and stroke if 3 or more standard drinks of alcohol are taken per day.…”

Section: Alcoholismmentioning

confidence: 99%

Molecular Studies on Coronary Artery Disease—A Review

Simon

Vijayakumar

2013

Ind J Clin Biochem

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Coronary artery disease (CAD) remains the major cause of mortality and morbidity in the entire world population. The conventional risk factors of CAD include hypertension, hyperlipidemia, diabetes mellitus, family history, smoking etc. These factors contribute only 50 % of the total risk of CAD. For providing a complete risk assessment in CAD, it is mandatory to have well-planned clinical, biochemical and genetic studies in patients with CAD and subjects who are at risk of developing CAD. In this review an attempt is made to critically evaluate the conventional and emerging risk factors which predispose the individual to CAD. Specifically, the molecular basis of CAD including high oxidative stress, low antioxidant status and increased DNA damage are covered. A comprehensive and multifactorial approach to the problem is the better way to reduce the morbidity and mortality of the disease.

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“…29 Genetic factors can determine how well alcohol is metabolized and can play a role in determining the interactions between alcohol and its metabolites and the heart. 30 For example, polymorphism of the alcohol dehydrogenase type 3 (ADH3) gene alters the rate of alcohol metabolism. It has been shown that moderate drinkers who are homozygous for the slow-oxidizing ADH3 allele have higher HDL levels and a decreased risk of myocardial infarction.…”

Section: Etiology and Pathophysiologymentioning

confidence: 99%