Ethanol-Associated Cardiomyocyte Apoptosis and Left Ventricular Dilation Are Unrelated to Changes in Myocardial Telomere Length in Rats

Raymond, Andrew; Becker, Jason R; Woodiwiss, Angela J.; Booysen, Hendrik L.; Norton, Gavin R.; Brooksbank, Richard

doi:10.1016/j.cardfail.2015.06.013

Cited by 8 publications

(8 citation statements)

References 57 publications

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“…For instance, chronic alcohol intake increased apoptotic bodies in hearts from humans (90), male and female mice (15, 57, 89, 92), and male rats (88, 93). Based on methodological variations it appears that apoptosis can be increased within as little as 6 wks (4% v/v liquid diet) in mice (57) and 4 months (5% v/v alcohol in drinking water) in rats (93). The use of Annexin V staining with fluorescence-activated cell sorting has confirmed an alcohol-mediated increase in apoptosis in cardiomyocytes (94, 95).…”

Section: Apoptosismentioning

confidence: 99%

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Steiner

Lang

2017

The International Journal of Biochemistry & Cell Biology

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Putative mechanisms leading to the development of alcoholic cardiomyopathy (ACM) include the interrelated cellular processes of mitochondria metabolism, oxidative stress and apoptosis. As mitochondria fuel the constant energy demands of this continually contracting tissue, it is not surprising that alcohol-induced molecular changes in this organelle contribute to cardiac dysfunction and ACM. As the causal relationship of these processes with ACM has already been established, the primary objective of this review is to provide an update of the experimental findings to more completely understand the aforementioned mechanisms. Accordingly, recent data indicate that alcohol impairs mitochondria function assessed by membrane potential and respiratory chain activity. Indictors of oxidative stress including superoxide dismutase, glutathione metabolites and malondialdehyde are also adversely affected by alcohol oftentimes in a sex-dependent manner. Additionally, myocardial apoptosis is increased based on assessment of TUNEL staining and caspase activity. Recent work has also emerged linking alcohol-induced oxidative stress with apoptosis providing new insight on the codependence of these interrelated mechanisms in ACM. Attention is also given to methodological differences including the dose of alcohol, experimental model system and the use of males versus females to highlight inconsistencies and areas that would benefit from establishment of a consistent model.

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Section: Apoptosismentioning

confidence: 99%

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Steiner

Lang

2017

The International Journal of Biochemistry & Cell Biology

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“…The data regarding the association between alcohol consumption and TL are inconsistent. Some studies show that alcohol abuse is associated with shortened telomeres suggesting a premature ageing at the cellular level (Pavanello et al 2011;Raymond et al 2016). Even minor alcohol consumption in midlife is significantly associated with shorter leukocyte TL in old age (Strandberg et al 2012).…”

Section: Alcoholism and Tlmentioning

confidence: 99%

Telomere length in psychiatric disorders: Is it more than an ageing marker?

Monroy-Jaramillo

Dyukova

Walss‐Bass

2017

The World Journal of Biological Psychiatry

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“…8 It is well accepted that apoptosis is one of the primary factors underlying aggravated pathogenesis of myocardial injury. Several studies have reported that ethanol can induce cardiomyocyte apoptosis, 3,22 by destroying the integrity of cardiomyocyte membranes, interfering with energy metabolism, increasing oxidative stress-mediated damage, and altering protein structure and thus function. 23,24 Several studies have demonstrated that ethanol-induced cardiomyocyte injury is alleviated through reduction of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Empagliflozin alleviates ethanol‐induced cardiomyocyte injury through inhibition of mitochondrial apoptosis via a SIRT1/PTEN/Akt pathway

Tian

Yang

Deng

et al. 2021

Clin Exp Pharma Physio

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Ethanol‐induced myocardial injury involves multiple pathophysiological processes including apoptosis. Empagliflozin (EMPA), is a novel hypoglycaemic drug which possesses multiple pharmacologically relevant protective effects, including anti‐apoptotic, anti‐inflammatory and antioxidant effects. However, whether EMPA treatment has a protective effect on ethanol‐induced myocardial injury has not been assessed, to the best of our knowledge. Therefore, the aim of this study was to determine the effect of EMPA treatment on ethanol‐induced myocardial injury and the underlying mechanism. An ethanol‐induced myocardial injury model was established by culturing H9c2 cells treated with 200 mmol/L ethanol for 24 hours, and additional groups of ethanol treated cells were also treated with EMPA with or without SIRT1 inhibitors prior to ethanol treatment. Cell viability and apoptosis were assessed using a CCK‐8 assay and flow cytometry, respectively. The expression of apoptosis‐related proteins was assessed using western blotting. The results showed that EMPA pretreatment resulted in increased cell viability and a decrease in LDH activity. Moreover, EMPA pretreatment significantly reduced apoptosis of cardiomyocytes, and reduced the expression of cleaved caspase 3. Furthermore, EMPA increased the expression of SIRT1, increased the phosphorylation levels of Akt, and reduced the expression of PTEN. EMPA also reduced ethanol‐induced mitochondrial apoptosis, increasing the Bcl‐2/Bax ratio and the mitochondrial membrane potential. However, the cardioprotective effects of EMPA were abrogated when cells were pretreated with a SIRT1 inhibitor. In conclusion, EMPA can alleviate ethanol‐induced myocardial injury by inhibiting mitochondrial apoptosis via the SIRT1/PTEN/Akt pathway. Therefore, EMPA may be a novel target for treatment of ethanol‐induced myocardial injury.

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Ethanol-Associated Cardiomyocyte Apoptosis and Left Ventricular Dilation Are Unrelated to Changes in Myocardial Telomere Length in Rats

Cited by 8 publications

References 57 publications

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

Telomere length in psychiatric disorders: Is it more than an ageing marker?

Empagliflozin alleviates ethanol‐induced cardiomyocyte injury through inhibition of mitochondrial apoptosis via a SIRT1/PTEN/Akt pathway

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