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Dissecting the molecular pathophysiology of drug-induced liver injury

World journal of Gastroenterology 2018年第13期24卷 1373-1385页

作者： Hui Ye Leonard j Nelson Manuel Gómez del Moral Eduardo Martínez-Naves francisco j.vier cubero Department of Immunology Ophtalmology and ORLComplutense University School of MedicineMadrid 28040Spain 12 de Octubre Health Research Institute(imas12) Madrid 28041Spain Institute for BioEngineering(Human Liver Tissue Engineering Faraday BuildingThe University of EdinburghThe King BuildingsMayfield RoadEdinburgh EH9 3 JLScotlandUnited Kingdom Department of Cell Biology Complutense University School of MedicineMadrid 28040Spain

Drug-induced liver injury(DILI) has become a major topic in the field of Hepatology and Gastroenterology. DILI can be clinically divided into three phenotypes: hepatocytic, cholestatic and mixed. Although the clinical manifestations of DILI are variable and the pathogenesis complicated, recent insights using improved preclinical models, have allowed a better understanding of the mechanisms that trigger liver damage. In this review, we will discuss the pathophysiological mechanisms underlying DILI. The toxicity of the drug eventually induces hepatocellular damage through multiple molecular pathways, including direct hepatic toxicity and innate and adaptive immune responses. Drugs or their metabolites, such as the common analgesic, acetaminophen, can cause direct hepatic toxicity through accumulation of reactive oxygen species and mitochondrial dysfunction. The innate and adaptive immune responses play also a very important role in the occurrence of idiosyncratic DILI. Furthermore, we examine common forms of hepatocyte death and their association with the activation of specific signaling pathways.

关键词： signaling pathways acetaminophen Drug-induced liver injury cell death reactive oxygen species

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Alcoholic liver disease:Utility of animal models

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World journal of Gastroenterology 2018年第45期24卷 5063-5075页

作者： Arantza Lamas-Paz Fengjie Hao Leonard j Nelson Maria Teresa Vázquez Santiago Canals Manuel Gómez del Moral Eduardo Martínez-Naves Yulia A Nevzorova francisco j.vier cubero Department of Immunology Ophthalmology and ORLComplutense University School of MedicineMadrid 28040Spain 12 de Octubre Health Research Institute(imas12) Madrid 28041Spain Institute for Bioengineering(IBioE) School of EngineeringFaraday BuildingThe University of EdinburghEdinburgh EH9 3 JLScotlandUnited Kingdom Department of Human Anatomy and Embryology Complutense University School of MedicineMadrid 28040Spain Instituto de Neurociencias Consejo Superior de Investigaciones CientíficasUniversidad Miguel HernándezSan Juan de Alicante 03550Spain Department of Cell Biology Complutense University School of MedicineMadrid 28040Spain Department of Genetics Physiology and MicrobiologyFaculty of BiologyUniversidad ComplutenseMadrid 28040Spain Department of Internal Medicine Ⅲ University Hospital RWTH AachenAachen 52062Germany

Alcoholic liver disease(ALD) is a major cause of acute and chronic liver injury. Extensive evidence has been accumulated on the pathological process of ALD during the past decades. However, effective treatment options for ALD are very limited due to the lack of suitable in vivo models that recapitulate the full spectrum of ALD. Experimental animal models of ALD, particularly rodents, have been used extensively to mimic human ALD. An ideal animal model should recapitulate all aspects of the ALD process, including significant steatosis, hepatic neutrophil infiltration, and liver injury. A better strategy against ALD depends on clear diagnostic biomarkers, accurate predictor(s) of its progression and new therapeutic approaches to modulate stop or even reverse the disease. Numerous models employing rodent animals have been established in the last decades to investigate the effects of acute and chronic alcohol exposure on the initiation and progression of ALD. Although significant progress has been made in gaining better knowledge on the mechanisms and pathology of ALD, many features of ALD are unknown, and require further investigation, ideally with improved animal models that more effectively mimic human ALD. Although differences in the degree and stages of alcoholic liver injury inevitably exist between animal models and human ALD, the acquisition and translational relevance will be greatly enhanced with the development of new and improved animal models of ALD.

关键词： Steatohepatitis Cirrhosis Hepatocellular carcinoma Alcoholic liver disease Reactive oxygen species

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Molecular epidemiology and putative origin of hepatitis C virus in random volunteers from Argentina

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World journal of Gastroenterology 2013年第35期19卷 5813-5827页

作者： Noemí del Pino josé Raúl Oubia francisco Rodríguez-Frías juan Ignacio Esteban María Buti Teresa Otero josep Gregori Damir García-Cehic Silvia Camos María cubero Rosario Casillas jaume Guàrdia Rafael Esteban josep Quer Apunlab Laboratories Institute of Medical Microbiology and Parasitology (IMPAM) UBA-CONICET Department of MicrobiologyParasitology and Immunology Faculty of Medicine University of Buenos Aires CIBER de Enfermedades Hepáticas y Digestivas (CIBERehd) del Instituto de Salud Carlos Ⅲ and Biochemistry Department Hospital Universitari Vall d’Hebrón (HUVH) CIBERehd del Instituto de Salud Carlos Ⅲ Autonomous University of Barcelona and Liver Unit Internal Medicine Lab. Malalties Hepatiques Vall d’Hebron Institut de Recerca (VHIR) Hospital Universitari Vall d’Hebrón (HUVH) Unitat de Diagnostic Molecular HUVH Liver Unit Internal Medicine Lab Malalties Hepatiques VHIR-HUVH Roche Diagnostics SL CIBERehd del Instituto de Salud Carlos Ⅲ Liver Unit Internal Medicine Lab MalaltiesHepatiques VHIR-HUVH Liver Unit and Biochemistry Department HUVH

AIM:To study the subtype prevalence and the phylogenetic relatedness of hepatitis C virus(HCV)sequences obtained from the Argentine general population,a large cohort of individuals was analyzed.METHODS:Healthy Argentinian volunteers(n=6251)from 12 provinces representing all geographical regions of the country were studied.All parents or legal guardians of individuals younger than 18 years provided informed written consent for participation.The corresponding written permission from all municipal authorities was obtained from each city or town where subjects were to be included.HCV RNA reverse transcription-polymerase chain reaction products were sequenced and phylogenetically analyzed.The 5’untranslated region(5’UTR)was used for RNA detection and initial genotype classification.The NS5B polymerase region,encompassing nt 8262-8610,was used for subtyping.RESULTS:An unexpectedly low prevalence of HCV infection in the general population(0.32%)was observed.Our data contrasted with previous studies that reported rates ranging from 1.5%to 2.5%,mainly performed in selected populations of blood donors or vulnerable groups.The latter values are in keeping with the prevalence reported by the 2007 Argentinian HCV Consensus(approximately 2%).HCV subtypes weredistributed as follows:1a(25%),1b(25%),2c(25%),3a(5%),and 2j(5%).Two isolates ascribed either to genotype 1(5%)or to genotype 3(5%)by 5’UTR phylogenetic analysis could not be subtyped.Subtype 1a sequences comprised a highly homogeneous population and clustered with United States sequences.Genotype1b sequences represented a heterogeneous population,suggesting that this genotype might have been introduced from different sources.Most subtype 2c sequences clustered close to the 2c reported from Italy and Southern France.CONCLUSION:HCV has a low prevalence of 0.32%in the studied general population of Argentina.The pattern of HCV introduction and transmission in Argentina appears to be a consequence of multiple events and different for each subtype.

关键词： Hepatitis C virus NS5B subtyping Molecular epidemiology Hepatitis C virus Argentina Hepatitis C virus 5’ untranslated region

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