Epidemiologic and laboratory animal studies over several decades show an association between alcohol consumption and atherosclerotic cardiovascular disease (ACVD). Many studies point to a protective effect of frequent low-to-moderate consumption but a harmful effect of heavy drinking and chronic alcohol abuse on arterial disease and its associated morbidity and mortality. Recent analyses (e.g., mendelian randomization) have highlighted methodological problems in some epidemiologic studies, (e.g. the confounding effects of sick quitters being classified as abstainers, and/or of coincident favorable lifestyle factors in low-risk drinkers) that challenge their findings, especially the purported cardioprotection of low level alcohol consumption. Such controversy about the validity of epidemiologic data, particularly in the absence of randomized controlled trials, emphasizes the importance of gaining a complete basic science understanding of the effects of alcohol, at different exposures/levels, on atherogenesis in vivo and on arterial cells involved in vitro and of the cell and molecular mechanisms involved.
ACVD is the number one killer of both men and women worldwide. Alcohol consumption is a common and modifiable behavior that reportedly affects ACVD, with controversial evidence of a biphasic effect. A better, basic science understanding, of the effects of alcoholic beverage components (ethanol, acetaldehyde, red wine polyphenols) on arterial and heart health is required.
Studies in animal models of CVD and in cell cultures have shed light on potentially important effects of different levels of alcohol. More such studies are required to get a clear understanding of how alcohol might impact atherosclerosis and heart health and the mechanisms involved. This information will increase understanding of how drinking affects health and may lead to the development of new therapies for ACVD.
The Topic Editors welcome all manuscript types investigating the mechanistic effects of alcohol (different levels and exposures of Ethanol and/or its primary metabolite acetaldehyde, and/or red wine components) on atherosclerotic plaque development and cardiomyopathy in humans, and in animal models, and using relevant cells in culture (EC, SMC, fibroblasts, stem cells, myocytes, monocytes/macrophages etc) to increase our understanding of the fundamental mechanisms involved.
Keywords:
alcohol, ethanol, acetaldehyde, red wine polyphenols, atherosclerosis, cardiomyopathy, vascular smooth muscle, Endothelial Cells, Vascular Pathology, ACVD, Cardiac, Immune Cells
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Epidemiologic and laboratory animal studies over several decades show an association between alcohol consumption and atherosclerotic cardiovascular disease (ACVD). Many studies point to a protective effect of frequent low-to-moderate consumption but a harmful effect of heavy drinking and chronic alcohol abuse on arterial disease and its associated morbidity and mortality. Recent analyses (e.g., mendelian randomization) have highlighted methodological problems in some epidemiologic studies, (e.g. the confounding effects of sick quitters being classified as abstainers, and/or of coincident favorable lifestyle factors in low-risk drinkers) that challenge their findings, especially the purported cardioprotection of low level alcohol consumption. Such controversy about the validity of epidemiologic data, particularly in the absence of randomized controlled trials, emphasizes the importance of gaining a complete basic science understanding of the effects of alcohol, at different exposures/levels, on atherogenesis in vivo and on arterial cells involved in vitro and of the cell and molecular mechanisms involved.
ACVD is the number one killer of both men and women worldwide. Alcohol consumption is a common and modifiable behavior that reportedly affects ACVD, with controversial evidence of a biphasic effect. A better, basic science understanding, of the effects of alcoholic beverage components (ethanol, acetaldehyde, red wine polyphenols) on arterial and heart health is required.
Studies in animal models of CVD and in cell cultures have shed light on potentially important effects of different levels of alcohol. More such studies are required to get a clear understanding of how alcohol might impact atherosclerosis and heart health and the mechanisms involved. This information will increase understanding of how drinking affects health and may lead to the development of new therapies for ACVD.
The Topic Editors welcome all manuscript types investigating the mechanistic effects of alcohol (different levels and exposures of Ethanol and/or its primary metabolite acetaldehyde, and/or red wine components) on atherosclerotic plaque development and cardiomyopathy in humans, and in animal models, and using relevant cells in culture (EC, SMC, fibroblasts, stem cells, myocytes, monocytes/macrophages etc) to increase our understanding of the fundamental mechanisms involved.
Keywords:
alcohol, ethanol, acetaldehyde, red wine polyphenols, atherosclerosis, cardiomyopathy, vascular smooth muscle, Endothelial Cells, Vascular Pathology, ACVD, Cardiac, Immune Cells
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.