Alcoholic (ethanol-containing) beverages are consumed by most societies in the world. Low-to-moderate levels of ethanol consumption have been shown to reduce the risk of cardiovascular diseases and atherosclerosis. The decreased risk is likely due to alcohol's favorable pleiotropic effects on lipids, adhesion molecules, platelet activation and oxidative stress. However, there is also an abundance of clinical, experimental and epidemiological evidence showing that chronic high-dose ethanol consumption increases mortality, cardiovascular complications and also the progression of atherosclerosis. This last phenomenon appears to be due to the metabolism of ethanol, that leads to the formation of acetaldehyde, which is oxidized to acetate, leading to the generation of reactive oxygen species (ROS) and a toxic effect of ethanol on the formation of the atherosclerosis plaque.We will here briefly review the mechanisms through which high intakes of ethanol induce the formation of atherosclerotic plaque, focusing on increased oxidative stress as the main underlying mechanism. © 2012 .

Alcohol and cardiovascular disease: Still unresolved underlying mechanisms / Carnevale, Roberto; Nocella, Cristina. - In: VASCULAR PHARMACOLOGY. - ISSN 1537-1891. - ELETTRONICO. - 57:2-4(2012), pp. 69-71. [10.1016/j.vph.2012.06.005]

Alcohol and cardiovascular disease: Still unresolved underlying mechanisms

CARNEVALE, Roberto;NOCELLA, CRISTINA
2012

Abstract

Alcoholic (ethanol-containing) beverages are consumed by most societies in the world. Low-to-moderate levels of ethanol consumption have been shown to reduce the risk of cardiovascular diseases and atherosclerosis. The decreased risk is likely due to alcohol's favorable pleiotropic effects on lipids, adhesion molecules, platelet activation and oxidative stress. However, there is also an abundance of clinical, experimental and epidemiological evidence showing that chronic high-dose ethanol consumption increases mortality, cardiovascular complications and also the progression of atherosclerosis. This last phenomenon appears to be due to the metabolism of ethanol, that leads to the formation of acetaldehyde, which is oxidized to acetate, leading to the generation of reactive oxygen species (ROS) and a toxic effect of ethanol on the formation of the atherosclerosis plaque.We will here briefly review the mechanisms through which high intakes of ethanol induce the formation of atherosclerotic plaque, focusing on increased oxidative stress as the main underlying mechanism. © 2012 .
2012
acetaldehyde; adhesion molecules; atherosclerosis; ethanol; oxidative stress
01 Pubblicazione su rivista::01a Articolo in rivista
Alcohol and cardiovascular disease: Still unresolved underlying mechanisms / Carnevale, Roberto; Nocella, Cristina. - In: VASCULAR PHARMACOLOGY. - ISSN 1537-1891. - ELETTRONICO. - 57:2-4(2012), pp. 69-71. [10.1016/j.vph.2012.06.005]
File allegati a questo prodotto
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/485475
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? 11
  • Scopus 22
  • ???jsp.display-item.citation.isi??? 23
social impact