Pre-endurance training prevents acute alcoholic liver injury in rats through the regulation of damaged mitochondria accumulation and mitophagy balance

Ma, Guodong; Liu, Yanhuan; Zhang, Qinglai; Zhang, Baoguo; Zhao, Ning; Wang, Qiuling; Wang, Xiaodi

doi:10.1007/s12072-014-9529-5

Cited by 12 publications

(13 citation statements)

References 41 publications

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“…Besides the protection against mitochondrial damage, it is more important to trigger mitophagy to eliminate in a timely manner the damaged mitochondria [ 38 ]. Many studies reported that both acute (4.5–5.0 g/kg.bw for 1–5 days) and chronic (36% of total calories for 10 weeks) ethanol administration stimulated mitophagy, a protective response in mitigating liver injury [ 5 , 10 , 11 ]. Our study provided direct evidence supporting suppressed mitophagy in the chronic ethanol feeding model.…”

Section: Discussionmentioning

confidence: 99%

“…Mitophagy suppression increased mitochondrial damage and further aggravated ethanol-induced liver disease, while enhancing mitophagy potentially protected against ethanol-imposed hepatotoxicity [ 5 , 9 ]. However, limited mitophagy activation failed to offer its hepatic protection in rats following five days of ethanol intake at a dose of 5 g/kg.bw [ 10 ]. Thus, loss of mitophagy capacity or limited induction of mitophagy might be the underlying initiating factor for ALD progression.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, loss of mitophagy capacity or limited induction of mitophagy might be the underlying initiating factor for ALD progression. Increasing evidence proved that mitophagy activation reduced acute and chronic ethanol-induced hepatotoxicity, revealing different levels of mitochondrial dysfunction [ 5 , 9 , 10 , 11 ]. Although direct evidence has yet to be sought, the status of mitophagy could be different between acute and chronic ethanol-induced liver damage.…”

Section: Introductionmentioning

confidence: 99%

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Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Zhang

et al. 2016

Nutrients

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Emerging evidence suggested mitophagy activation mitigates ethanol-induced liver injury. However, the effect of ethanol on mitophagy is inconsistent. Importantly, the understanding of mitophagy status after chronic ethanol consumption is limited. This study evaluated the effect of quercetin, a naturally-occurring flavonoid, on chronic ethanol-induced mitochondrial damage focused on mitophagy. An ethanol regime to mice for 15 weeks (accounting for 30% of total calories) led to significant mitochondrial damage as evidenced by changes of the mitochondrial ultrastructure, loss of mitochondrial membrane potential and remodeling of membrane lipid composition, which was greatly attenuated by quercetin (100 mg/kg.bw). Moreover, quercetin blocked chronic ethanol-induced mitophagy suppression as denoted by mitophagosomes-lysosome fusion and mitophagy-related regulator elements, including LC3II, Parkin, p62 and voltage-dependent anion channel 1 (VDAC1), paralleling with increased FoxO3a nuclear translocation. AMP-activated protein kinase (AMPK) and extracellular signal regulated kinase 2 (ERK2), instead of AKT and Sirtuin 1, were involved in quercetin-mediated mitophagy activation. Quercetin alleviated ethanol-elicited mitochondrial damage through enhancing mitophagy, highlighting a promising preventive strategy for alcoholic liver disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Zhang

et al. 2016

Nutrients

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“…The effects of alcohol on mitophagy depend on the duration and amount of alcohol exposure. Increased mitophagy was reported in an acute alcohol binge rat model, which can be mediated by either the PINK1/Parkin or BNIP3 signaling pathways [119,120]. Hepatocellular mitochondria depolarize broadly to facilitate hepatic ethanol metabolism after immediate alcohol administration, which triggers a series of mitophagy regulating signals to promote mitophagy as a compensative response [121].…”

Section: Mitophagy In Aldmentioning

confidence: 99%

Role and Mechanisms of Mitophagy in Liver Diseases

McKeen

Zhang

et al. 2020

Cells

178

122

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The mitochondrion is an organelle that plays a vital role in the regulation of hepatic cellular redox, lipid metabolism, and cell death. Mitochondrial dysfunction is associated with both acute and chronic liver diseases with emerging evidence indicating that mitophagy, a selective form of autophagy for damaged/excessive mitochondria, plays a key role in the liver’s physiology and pathophysiology. This review will focus on mitochondrial dynamics, mitophagy regulation, and their roles in various liver diseases (alcoholic liver disease, non-alcoholic fatty liver disease, drug-induced liver injury, hepatic ischemia-reperfusion injury, viral hepatitis, and cancer) with the hope that a better understanding of the molecular events and signaling pathways in mitophagy regulation will help identify promising targets for the future treatment of liver diseases.

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“…Further, alcohol reduced glucose tolerance and increased the levels of TNF-α, IL-6, VEGF, and leptin [53]. Interestingly, one of the main characteristics of chronic and acute alcohol consumption is increased hepatic triglycerides [55], which are transported from adipose tissues to the liver and contribute to alcohol-induced fatty liver [52]. The mechanisms by which ethanol consumption results in elevated HIF-1α in adipose tissue have not been definitively concluded.…”

Section: The Role Of Hif-1α In Alcohol-mediated Adipose Damagementioning

confidence: 99%

Role of HIF-1α in Alcohol-Mediated Multiple Organ Dysfunction

Morris

Yeligar

2018

Biomolecules

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Excess alcohol consumption is a global crisis contributing to over 3 million alcohol-related deaths per year worldwide and economic costs exceeding $200 billion dollars, which include productivity losses, healthcare, and other effects (e.g., property damages). Both clinical and experimental models have shown that excessive alcohol consumption results in multiple organ injury. Although alcohol metabolism occurs primarily in the liver, alcohol exposure can lead to pathophysiological conditions in multiple organs and tissues, including the brain, lungs, adipose, liver, and intestines. Understanding the mechanisms by which alcohol-mediated organ dysfunction occurs could help to identify new therapeutic approaches to mitigate the detrimental effects of alcohol misuse. Hypoxia-inducible factor (HIF)-1 is a transcription factor comprised of HIF-1α and HIF-1β subunits that play a critical role in alcohol-mediated organ dysfunction. This review provides a comprehensive analysis of recent studies examining the relationship between HIF-1α and alcohol consumption as it relates to multiple organ injury and potential therapies to mitigate alcohol’s effects.

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Pre-endurance training prevents acute alcoholic liver injury in rats through the regulation of damaged mitochondria accumulation and mitophagy balance

Abstract: Pre-endurance training can decrease acute alcohol intake-induced damaged mitochondria accumulation and reduced acute alcohol intake-induced mitophagy, which built a new balance between mitophagy and damaged mitochondria accumulation.

Cited by 12 publications

References 41 publications

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy

Role and Mechanisms of Mitophagy in Liver Diseases

Role of HIF-1α in Alcohol-Mediated Multiple Organ Dysfunction

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