Alcoholic Myopathy in Heart and Skeletal Muscle

Bleich, Howard L.; Moore, Mary Jean; Rubin, Emanuel

doi:10.1056/nejm197907053010107

Cited by 189 publications

(12 citation statements)

References 29 publications

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“…The results from our study demonstrated that murine myocardia underwent a considerable number of adverse ultrastructural, structural, and histological changes following chronic alcohol consumption. In the present study, myocardial changes were found in the chronic alcohol-fed mice, such as fatty acid accumulation, cardiomyocyte vacuolization, myocardial myofibril loss and disarray, sarcoplasmic reticulum edema, and swollen disrupted mitochondria, which are consistent with those of previous reports [31-33]. The mechanisms underlying ACM include oxidative stress [4, 5], impaired mitochondrial bioenergetics [2], and derangements in fatty acid metabolism and transport [6].…”

Section: Discussionsupporting

confidence: 90%

Expression Profiling of Circular RNAs and Micrornas in Heart Tissue of Mice with Alcoholic Cardiomyopathy

Yang

Chen

Ding

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic heavy alcohol consumption may result in alcoholic cardiomyopathy. This study was designed to screen differentially expressed microRNAs and circular RNAs in heart tissue of mice with alcoholic cardiomyopathy to reveal the underlying molecular mechanism. Methods: Having established a murine alcoholic cardiomyopathy model, we screened differentially expressed microRNAs and circular RNAs in three heart samples from the alcohol-treated and control groups by high-throughput microarray analysis. We analyzed the function and biological signaling pathways of differentially expressed non-coding RNAs closely related to alcoholic cardiomyopathy using bioinformatics software to identify some mRNAs and their biological signaling pathways closely related to alcoholic cardiomyopathy. Results: Nineteen microRNAs and 265 circular RNAs were differentially expressed in the alcohol-treated group compared with the control group. After analyzing gene function and signaling pathways by bioinformatics software, we found that the differentially expressed mRNAs were associated with carbohydrate metabolism. Conclusions: Chronic alcohol consumption can change the non-coding RNA profile of heart tissue, which is closely related to the pathological mechanisms of alcoholic cardiomyopathy.

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Section: Discussionsupporting

confidence: 90%

Expression Profiling of Circular RNAs and Micrornas in Heart Tissue of Mice with Alcoholic Cardiomyopathy

Yang

Chen

Ding

et al. 2018

Cell Physiol Biochem

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“…Abnormalities of mitochondrial structure and function are known results of chronic EtOH abuse in both man and animals [70-72]. While some reports attribute this to acetaldehyde, the initial breakdown product of EtOH [71], others implicate cardiac metabolism of EtOH to FAEEs, which accumulate in the heart after chronic EtOH exposure, bind to mitochondria, and interfere with mitochondrial ATP production.…”

Section: Discussionmentioning

confidence: 99%

Chronic ethanol consumption increases cardiomyocyte fatty acid uptake and decreases ventricular contractile function in C57BL/6J mice

Hyodo

et al. 2013

Journal of Molecular and Cellular Cardiology

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Alcohol, a major cause of human cardiomyopathy, decreases cardiac contractility in both animals and man. However, key features of alcohol-related human heart disease are not consistently reproduced in animal models. Accordingly, we studied cardiac histology, contractile function, cardiomyocyte long chain fatty acid (LCFA) uptake, and gene expression in male C57BL/6J mice consuming 0, 10, 14, or 18% ethanol in drinking water for 3 months. At sacrifice, all EtOH groups had mildly decreased body and increased heart weights, dose-dependent increases in cardiac triglycerides and a marked increase in cardiac fatty acid ethyl esters. [3H]-oleic acid uptake kinetics demonstrated increased facilitated cardiomyocyte LCFA uptake, associated with increased expression of genes encoding the LCFA transporters CD36 and Slc27a1 (FATP1) in EtOH-fed animals. Although SCD-1 expression was increased, lipidomic analysis did not indicate significantly increased de novo LCFA synthesis. By echocardiography, ejection fraction (EF) and the related fractional shortening (FS) of left ventricular diameter during systole were reduced and negatively correlated with cardiac triglycerides. Expression of myocardial PGC-1α and multiple downstream target genes in the oxidative phosphorylation pathway, including several in the electron transport and ATP synthase complexes of the inner mitochondrial membrane, were down-regulated. Cardiac ATP was correspondingly reduced. The data suggest that decreased expression of PGC-1α and its target genes result in decreased cardiac ATP levels, which may explain the decrease in myocardial contractile function caused by chronic EtOH intake. This model recapitulates important features of human alcoholic cardiomyopathy and illustrates a potentially important pathophysiologic link between cardiac lipid metabolism and function.

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“…Since alcoholic myopathy arises in the presence or absence of polyneuropathy [98], the two disease processes should be evaluated independently. Alcoholic myopathy is a progressive disease that impairs strength due to loss of lean tissue and worsens with duration and level of alcohol abuse [129, 131, 159, 160]. Myofiber atrophy can result in 30 % loss in muscle mass [119].…”

Section: Neuromuscular Diseases In Alcoholicsmentioning

confidence: 99%

Human alcohol-related neuropathology

2013

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Alcohol-related diseases of the nervous system are caused by excessive exposures to alcohol, with or without co-existing nutritional or vitamin deficiencies. Toxic and metabolic effects of alcohol (ethanol) vary with brain region, age/developmental stage, dose, and duration of exposures. In the mature brain, heavy chronic or binge alcohol exposures can cause severe debilitating diseases of the central and peripheral nervous systems, and skeletal muscle. Most commonly, long-standing heavy alcohol abuse leads to disproportionate loss of cerebral white matter and impairments in executive function. The cerebellum (especially the vermis), cortical-limbic circuits, skeletal muscle, and peripheral nerves are also important targets of chronic alcohol-related metabolic injury and degeneration. Although all cell types within the nervous system are vulnerable to the toxic, metabolic, and degenerative effects of alcohol, astrocytes, oligodendrocytes, and synaptic terminals are major targets, accounting for the white matter atrophy, neural inflammation and toxicity, and impairments in synaptogenesis. Besides chronic degenerative neuropathology, alcoholics are predisposed to develop severe potentially life-threatening acute or subacute symmetrical hemorrhagic injury in the diencephalon and brainstem due to thiamine deficiency, which exerts toxic/metabolic effects on glia, myelin, and the microvasculature. Alcohol also has devastating neurotoxic and teratogenic effects on the developing brain in association with fetal alcohol spectrum disorder/fetal alcohol syndrome. Alcohol impairs function of neurons and glia, disrupting a broad array of functions including neuronal survival, cell migration, and glial cell (astrocytes and oligodendrocytes) differentiation. Further progress is needed to better understand the pathophysiology of this exposure-related constellation of nervous system diseases and better correlate the underlying pathology with in vivo imaging and biochemical lesions.

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Alcoholic Myopathy in Heart and Skeletal Muscle

Cited by 189 publications

References 29 publications

Expression Profiling of Circular RNAs and Micrornas in Heart Tissue of Mice with Alcoholic Cardiomyopathy

Expression Profiling of Circular RNAs and Micrornas in Heart Tissue of Mice with Alcoholic Cardiomyopathy

Chronic ethanol consumption increases cardiomyocyte fatty acid uptake and decreases ventricular contractile function in C57BL/6J mice

Human alcohol-related neuropathology

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