Cardioprotection by Regular Ethanol Consumption: Potential Mechanisms and Clinical Application

Miyamae, Masami; Kaneda, Kazuhiro; Domae, Naochika; Figueredo, Vincent M.

doi:10.2174/1874473711003010039

Cited by 19 publications

(14 citation statements)

References 129 publications

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“…Quadratic models are often found to best explain biological phenomena. For example, U-shaped models are often used to describe the relationship between ethanol intake and risk of myocardial infarction (i.e., lower risk of myocardial infarction in individuals with light to moderate consumption) [33] and the relationship between cholesterol intake and mortality (both low and high cholesterol are associated with increased risk of mortality) [34]. …”

Section: Discussionmentioning

confidence: 99%

Torpedo Formation and Purkinje Cell Loss: Modeling their Relationship in Cerebellar Disease

et al. 2014

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Background Torpedo formation and Purkinje cell (PC) loss represent standard and inter-related cerebellar responses to injury. Surprisingly, the nature of their relationship has not been carefully characterized across a range of normal and disease states. Are brains with more torpedoes expected to have fewer PCs? We quantified torpedoes and PCs in four groups: essential tremor (ET), spinocerebellar ataxia (SCA), multiple system atrophy-cerebellar (MSA-C), and controls. Methods Brains from 100 individuals (58 ET, 27 controls, 7 SCA, 8 MSA-C) were available at the New York Brain Bank. After complete neuropathological assessment, a standard parasagittal neocerebellar block was harvested, a 7-μm thick section was stained with Luxol Fast Blue/Hematoxylin and Eosin, and torpedoes and PCs were quantified. Results For a given PC count, SCA and MSA-C cases often had higher torpedo counts than ET cases or controls. Furthermore, the relationship between torpedo and PC counts was complex. The correlation between torpedo and PC counts was negative in ET cases (i.e., individuals with more torpedoes had fewer PCs [i.e., more PC loss]) whereas the relationship was positive in MSA-C cases (i.e., individuals with fewer PCs [i.e., more PC loss] had fewer torpedoes). Patients with SCA showed both patterns. When all diagnostic groups were combined, the correlation was best fit by a quadratic (i.e. parabolic) model rather than a simple linear model; this model incorporated data on the negative correlation in ET cases, the mixed results in SCA cases, and the positive correlation in MSA-C cases (r = 0.636). Conclusions The relationship between torpedo and PC counts was complex and heterogeneous across a range of cerebellar disease states, and was best characterized by a quadratic rather than a simple model. With more severe cerebellar disease, torpedoes can be quite numerous, and are likely a common feature of surviving PCs, but eventually, dramatic loss of PC leads to a paradoxical reduction in observable torpedoes.

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Section: Discussionmentioning

confidence: 99%

Torpedo Formation and Purkinje Cell Loss: Modeling their Relationship in Cerebellar Disease

et al. 2014

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“…16 Alcohol has been shown to attenuate ischemia-reperfusion injury and improve outcomes and survival after myocardial infarction. 2, 17 Animal studies have revealed that moderate alcohol consumption protects against ischemic insult by “ethanol preconditioning”, which renders the myocardium more resistant to ischemia reperfusion injury. 18, 19 In this study, alcohol reduced apoptosis signaling, decreased cell death and improved cell survival in both the ischemic and non-ischemic myocardium.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Consumption Mitigates Apoptosis and Mammalian Target of Rapamycin Signaling in Myocardium

Elmadhun

Sabe

Lassaletta

et al. 2014

Journal of the American College of Surgeons

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Background Epidemiologic studies have shown that individuals who consume low to moderate alcohol have a lower risk of developing cardiovascular disease compared to abstainers. Although experimental studies confirmed this observation, the effect of alcohol on ischemic myocardium is still unclear. We developed a clinically relevant animal model of chronic myocardial ischemia to investigate the effects of moderate alcohol consumption on the myocardium. Study Design Fourteen Yorkshire swine underwent placement of an ameroid constrictor to induce chronic myocardial ischemia. Postoperatively, one group was supplemented with 90mL 50% ethanol daily (ETOH n=7), and one group was supplemented with 80g of sucrose daily to normalize caloric intake between groups (SUC n=7). After 7 weeks, all animals underwent sternotomy, and harvest of the chronically ischemic myocardium and non-ischemic myocardium. Tissues were analyzed for protein expression and stained for apoptosis quantification. Results In the ischemic myocardium, alcohol down-regulated pro-apoptotic proteins TNFα, FOX03, BAD and caspase 9, up-regulated pro-survival proteins AMPK, pAMPK and pFOX03, and down regulated MTOR signaling by down regulating MTOR, pMTOR and up-regulating Deptor. In the non-ischemic myocardium, alcohol up-regulated pro-survival proteins AKT, pAKT, pBCL2, AMPK, pBAD, pFOX03 and down regulated MTOR signaling by down regulating pMTOR and up-regulating Deptor. Alcohol also decreased cell death as measured by TUNEL staining in the ischemic and non-ischemic myocardium. Conclusions Alcohol consumption down regulates apoptosis and promotes cell survival in the ischemic and non-ischemic myocardium. Alcohol also modulates MTOR signaling, which regulates senescence and apoptosis. Perhaps MTOR and apoptosis regulation is another mechanism by which moderate ethanol consumption is cardioprotective.

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“…Acute exposure to other nucleoside transport inhibitors, including dilazep [10] and ethanol [11], also mimic or enhance the protective effect of ischemic preconditioning against ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Regular dipyridamole therapy produces sustained protection against cardiac ischemia–reperfusion injury: Is it time to revisit PARIS?

Figueredo

Okusa

Kaneda

et al. 2014

International Journal of Cardiology

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Cardioprotection by Regular Ethanol Consumption: Potential Mechanisms and Clinical Application

Cited by 19 publications

References 129 publications

Torpedo Formation and Purkinje Cell Loss: Modeling their Relationship in Cerebellar Disease

Torpedo Formation and Purkinje Cell Loss: Modeling their Relationship in Cerebellar Disease

Alcohol Consumption Mitigates Apoptosis and Mammalian Target of Rapamycin Signaling in Myocardium

Regular dipyridamole therapy produces sustained protection against cardiac ischemia–reperfusion injury: Is it time to revisit PARIS?

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