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

Wang, S; Pacher, Pál; Rc, De Lisle; Huang, Heqing; Wx, Ding

doi:10.1111/acer.13078

Cited by 106 publications

(101 citation statements)

References 89 publications

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“…Additional aberrant processes, such as circadian rhythms, 80 autophagy, 81 and ER stress 82 are associated with pathogenesis of ALD. Both adiponectin and FGF15/19 are involved in regulating circadian rhythms, 83,84 autophagy 85,86 and ER stress 87,88 .…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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“…1 Both intrinsic and extrinsic apoptosis are involved in cholestatic liver injury, alcoholic and nonalcoholic steatohepatitis (ASH and NASH), and milder hepatotoxic injury. 2,3,8 The family of dependence receptors encompasses around 20 members which include netrin1 receptors (DCC and UNC5A-D), neurotrophin receptor (NTRK3), and the sonic hedgehog receptor patched. Although ligand-mediated activation of these dependence receptors promotes cell proliferation, differentiation, and survival, the ligand depletion triggers death pathways via CASP9-CASP3 activation or a p53-dependent mechanism.…”

Section: Apoptosismentioning

confidence: 99%

“…1 These different types of death may be manifested by hepatocytes, biliary epithelial cells, or non-parenchymal liver cells in a manner dependent on etiology, the nature and extent of co-morbidities, and disease stage. 2,3…”

Section: Introductionmentioning

confidence: 99%

Cell Death and Liver Disease

2020

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Cell death is now reclassified into several types based on the mechanisms and morphologic phenotype. Understanding of such classifications offers insights into the pathogenesis of liver disease, as well as diagnostic or therapeutic implications. Apoptosis is recognized relatively easily due to its unique morphology, but lytic cell death may occur in the form of accidental necrosis, mitochondria permeability transitiondriven necrosis, necroptosis, pyroptosis, ferroptosis, and parthanatos. The cell may be engulfed by neighboring cells due to a loss of integrin signaling or cancer cell competition by entosis, a type of cell death. The classification also includes mechanistically termed cell death such as autophagy-dependent cell death and lysosome-dependent cell death. These different types of cell death may occur uniquely in certain liver diseases but may coexist in the evolution of the disease. They occur in parenchymal and non-parenchymal liver cells, as well as inflammatory cells, causing distinct pathologic consequences. This review briefly covers the recently revised classifications of cell death and discusses their relevance to liver diseases of different etiologies.

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“…Autophagy has been reported to participate in digestive system diseases. In alcoholic liver disease, which is caused by chronic alcohol consumption and the subsequently increased production of highly reactive acetaldehyde, ROS, and fatty acid ethyl esters, autophagy serves as a cleaner to eliminate these wastes. However, long‐term alcohol consumption inhibits autophagy via elevation of lysosomal pH and alteration of trafficking of lysosomal enzymes .…”

Section: Landscape Of Aads In Humansmentioning

confidence: 99%

Modulation of autophagy in human diseases strategies to foster strengths and circumvent weaknesses

Sui

Zhang

et al. 2019

Medicinal Research Reviews

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Autophagy is central to the maintenance of intracellular homeostasis across species. Accordingly, autophagy disorders are linked to a variety of diseases from the embryonic stage until death, and the role of autophagy as a therapeutic target has been widely recognized. However, autophagy‐associated therapy for human diseases is still in its infancy and is supported by limited evidence. In this review, we summarize the landscape of autophagy‐associated diseases and current autophagy modulators. Furthermore, we investigate the existing autophagy‐associated clinical trials, analyze the obstacles that limit their progress, offer tactics that may allow barriers to be overcome along the way and then discuss the therapeutic potential of autophagy modulators in clinical applications.

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

Cited by 106 publications

References 89 publications

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

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

Cell Death and Liver Disease

Modulation of autophagy in human diseases strategies to foster strengths and circumvent weaknesses

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