Role of Mitochondria in Alcoholic Liver Disease

Garcı́a-Ruiz, Carmen; Kaplowitz, Neil; Fernández‐Checa, José C.

doi:10.1007/s40139-013-0021-z

Cited by 56 publications

(52 citation statements)

References 104 publications

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“…Acute and chronic alcohol exposure alter liver mitochondria structure and function in animal models and humans 25 . Alcohol exposure also damages mitochondrial DNA and ribosomes and decreases rates of mitochondrial respiration (state III) and oxygen consumption, leading to mitochondrial-mediated apoptosis 11, 26 .…”

Section: Mitochondria Endoplasmic Reticulum (Er) Stress and Autophagymentioning

confidence: 99%

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

et al. 2016

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Alcoholic liver disease (ALD) develops in approximately 20% of alcoholics, with a higher prevalence in females. ALD progression is marked by fatty liver and hepatocyte necrosis, as well as apoptosis, inflammation, regenerating nodules, fibrosis, and cirrhosis 1. ALD develops via a complex process involving parenchymal and non-parenchymal cells, as well as recruitment of other cell types to the liver in response to damage and inflammation. Hepatocytes are damaged by ethanol, via generation of reactive oxygen species and induction of endoplasmic reticulum stress and mitochondrial dysfunction. Hepatocyte cell death via apoptosis and necrosis are markers of ethanol-induced liver injury. We review the mechanisms by which alcohol injures hepatocytes and the response of hepatic sinusoidal cells to alcohol-induced injury. We also discuss how recent insights into the pathogenesis of ALD will affect treatment and management of patients.

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Section: Mitochondria Endoplasmic Reticulum (Er) Stress and Autophagymentioning

confidence: 99%

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

et al. 2016

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“…71,72 Given the beneficial functions of adiponectin and FGF15/19 on mitochondria and liver, adiponectin-FGF15/19 signaling may protect liver from ethanol-induced injury through rescuing mitochondria. In addition, mitochondria are the major source of ROS in non-phagocytic cells like hepatocytes.…”

Section: Adiponectin-fgf15/19 Signaling Improves Mitochondrial Functionmentioning

confidence: 99%

Endocrine Adiponectin‐FGF15/19 Axis in Ethanol-Induced Inflammation and Alcoholic Liver Injury

et al. 2018

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Alcoholic liver disease (ALD) is the most prevalent form of liver diseases, encompassing a spectrum of progressive pathological changes from steatosis to steatohepatitis to fibrosis/cirrhosis and hepatocellular carcinoma. Alcoholic steatosis/steatohepatitis is the initial stage of ALD and a major risk factor for advanced liver injuries. Adiponectin is a hormone secreted from adipocytes. Fibroblast growth factor (FGF) 15 (human homolog, FGF19) is an ileum-derived hormone. Adipocyte-derived adiponectin and gut-derived FGF15/19 regulate each other, share common signaling cascades and exert similar beneficial functions. Emerging evidence has revealed that dysregulated adiponecitn-FGF15/19 axis and impaired hepatic adiponectin-FGF15/19 signaling are associated with alcoholic liver damage in rodents and humans. More importantly, endocrine adiponectin-FGF15/19 signaling confers protection against ethanol-induced liver damage via fine-tuning the adipose-intestine-liver crosstalk, leading to limited hepatic inflammatory responses, and ameliorated alcoholic liver injury. This review is focused on the recently discovered endocrine adiponectin-FGF15/19 axis that is emerging as an essential adipose-gut-liver coordinator involved in the development and progression of alcoholic steatohepatitis.

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“…The finding that depolarized mitochondria in mouse liver are reversible is very intriguing, suggesting that mitochondria may adapt to ethanol-induced damage. Indeed, it has been well documented that acute or chronic alcohol exposure can alter liver mitochondria structures (e.g., enlarged mitochondria) and functions in both animal models and human alcoholics (Garcia-Ruiz et al, 2013). Several adaptive mechanisms in the liver can be activated in response to acute or chronic alcohol-induced mitochondrial damage and metabolic stress.…”

Section: Activation Of Mitochondrial (Intrinsic) Apoptotic Pathway Bymentioning

confidence: 99%

A Mechanistic Review of Cell Death in Alcohol‐Induced Liver Injury

Wang

Pacher

et al. 2016

Alcoholism Clin & Exp Res

108

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Alcoholic liver disease is a major health problem in the United States and worldwide without successful treatments. Chronic alcohol consumption can lead to alcoholic liver disease (ALD), which is characterized by steatosis, inflammation, fibrosis, cirrhosis and even liver cancer. Recent studies suggest that alcohol induces both cell death and adaptive cell survival pathways in the liver, and the balance of cell death and cell survival ultimately decides the pathogenesis of ALD. This review summarizes the recent progress on the role and mechanisms of apoptosis, necroptosis and autophagy in the pathogenesis of ALD. Understanding the complex regulation of apoptosis, necrosis and autophagy may help to develop novel therapeutic strategies by targeting all three pathways simultaneously.

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Role of Mitochondria in Alcoholic Liver Disease

Cited by 56 publications

References 104 publications

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes

Endocrine Adiponectin‐FGF15/19 Axis in Ethanol-Induced Inflammation and Alcoholic Liver Injury

A Mechanistic Review of Cell Death in Alcohol‐Induced Liver Injury

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