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| 1 | Bile acid metabolism and signaling in liver disease and therapy显示文摘Bile acids play a critical role in the regulation of glucose,lipid,and energy metabolism through activation of the nuclear bile acid receptor farnesoid X receptor(FXR)and membrane G protein-coupled bile acid receptor-1(Gpbar-1,aka TGR5).Agonist activation of FXR and TGR5 improves insulin and glucose sensitivity and stimulates energy metabolism to prevent diabetes,obesity,and non-alcoholic fatty liver disease(NAFLD).Bile acids have both pro-and anti-inflammatory actions through FXR and TGR5 in the intestine and liver.In the intestine,bile acids activate FXR and TGR5 to stimulate fibroblast growth factor 15 and glucagon-like peptide-1 secretion.FXR and TGR5 agonists may have therapeutic potential for treating liver-related metabolic diseases,such as diabetes and NAFLD. | John Y.L.Chiang | 2017 | Liver Research2017，1，1： | 18 |
| 2 | Gut microbiota,fatty liver disease,and hepatocellular carcinoma显示文摘Intestinal bacteria contribute to the pathogenesis of non-alcoholic fatty liver disease(NAFLD).Recently developed microbial profiling techniques are beginning to shed light on the nature of the changes in the gut microbiota that accompany NAFLD and non-alcoholic steatohepatitis(NASH).In this review,we summarize the role of gut microbiota in the development of NAFLD,NASH,and hepatocellular carcinoma(HCC).We highlight the mechanisms by which gut microbiota contribute to NAFLD/NASH,including through alterations in gut epithelial permeability,choline metabolism,endogenous alcohol production,release of inflammatory cytokines,regulation of hepatic Toll-like receptor(TLR),and bile acid metabolism.In addition,we analyze possible mechanisms for enhanced hepatic carcinogenesis,including alterations in bile acid metabolism,release of inflammatory cytokines,and expression of TLR-4.Finally,we describe therapeutic approaches for NAFLD/NASH and preventive strategies for HCC involving modulation of the intestinal microbiota or affected host pathways.Although recent studies have provided useful information,large-scale prospective studies are required to better characterize the intestinal microbiota and metabolome,in order to demonstrate a causative role for changes in the gut microbiota in the etiology of NAFLD/NASH,to identify new therapeutic strategies for NAFLD/NASH,and to develop more effective methods of preventing HCC. | Huikuan Chu Brandon Williams Bernd Schnabl | 2018 | Liver Research2018，2，1： | 16 |
| 3 | Alcoholic liver disease: A current molecular and clinical perspective显示文摘Heavy alcohol use is the cause of alcoholic liver disease(ALD).The ALD spectrum ranges from alcoholic steatosis to steatohepatitis,fibrosis,and cirrhosis.In Western countries,approximately 50%of cirrhosis-related deaths are due to alcohol use.While alcoholic cirrhosis is no longer considered a completely irreversible condition,no effective anti-fibrotic therapies are currently available.Another significant clinical aspect of ALD is alcoholic hepatitis(AH).AH is an acute inflammatory condition that is often comorbid with cirrhosis,and severe AH has a high mortality rate.Therapeutic options for ALD are limited.The established treatment for AH is corticosteroids,which improve short-term survival but do not affect long-term survival.Liver transplantation is a curative treatment option for alcoholic cirrhosis and AH,but patients must abstain from alcohol use for 6 months to qualify.Additional effective therapies are needed.The molecular mechanisms underlying ALD are complex and have not been fully elucidated.Various molecules,signaling pathways,and crosstalk between multiple hepatic and extrahepatic cells contribute to ALD progression.This review highlights established and emerging concepts in ALD clin-icopathology,their underlying molecular mechanisms,and current and future ALD treatment options. | Koichiro Ohashi Michael Pimienta Ekihiro Seki | 2018 | Liver Research2018，2，4： | 15 |
| 4 | Autophagy in non-alcoholic fatty liver disease and alcoholic liver disease显示文摘Autophagy is an evolutionarily conserved intracellular degradative function that is important for liver homeostasis.Accumulating evidence suggests that autophagy is deregulated during the progression and development of alcoholic and non-alcoholic liver diseases.Impaired autophagy prevents the clearance of excessive lipid droplets(LDs),damaged mitochondria,and toxic protein aggregates,which can be generated during the progression of various liver diseases,thus contributing to the development of steatosis,injury,steatohepatitis,fibrosis,and tumors.In this review,we look at the status of hepatic autophagy during the pathogenesis of alcoholic and non-alcoholic liver diseases.We also examine the mechanisms of defects in autophagy,and the hepato-protective roles of autophagy in non-alcoholic fatty liver disease(NAFLD)and alcoholic liver disease(ALD),focusing mainly on steatosis and liver injury.Finally,we discuss the therapeutic potential of autophagy modulating agents for the treatment of these two common liver diseases. | Bilon Khambu Shengmin Yan Nazmul Huda Gang Liu Xiao-Ming Yin | 2018 | Liver Research2018，2，3： | 13 |
| 5 | Bile acid receptors and gastrointestinal functions显示文摘Bile acids modulate several gastrointestinal(GI)functions including electrolyte secretion and absorption,gastric emptying,and small intestinal and colonic motility.High concentrations of bile acids lead to diarrhea and are implicated in the development of esophageal,gastric and colonic cancer.Alterations in bile acid homeostasis are also implicated in the pathophysiology of irritable bowel syndrome(IBS)and inflammatory bowel disease(IBD).Our understanding of the mechanisms underlying these effects of bile acids on gut functions has been greatly enhanced by the discovery of bile acid receptors,including the nuclear receptors:farnesoid X receptor(FXR),vitamin D receptor(VDR),pregnane X receptor(PXR),and constitutive androstane receptor(CAR);and G protein-coupled receptors(GPCRs):Takeda G protein-coupled receptor 5(TGR5),sphingosine-1-phosphate receptor 2(S1PR2),and muscarinic acetylcholine receptor M3(M3R).For example,various studies provided evidence demonstrating the anti-inflammatory effects of FXR and TGR5 activation in models of intestinal inflammation.In addition,the activation of TGR5 in enteric neurons was recently shown to increase colonic motility,which may lead to bile acid-induced diarrhea(BAD).Interestingly,TGR5 induces the secretion of glucagon-like peptide-1(GLP-1)from L-cells to enhance insulin secretion and modulate glucose metabolism.Because of the importance of these receptors,agonists of TGR5 and intestine-specific FXR agonists are currently being tested as an option for the treatment of diabetes mellitus and primary bile acid diarrhea,respectively.This review summarizes current knowledge of the functional roles of bile acid receptors in the GI tract. | Alexander L.Ticho Pooja Malhotra Pradeep K.Dudeja Ravinder K.Gill Waddah A.Alrefai | 2019 | Liver Research2019，3，1： | 13 |
| 6 | The role of gut microbiota in liver disease development and treatment显示文摘Liver cancer is the sixth most common cancer worldwide,and the third most common cause of cancer-related death.Hepatocellular carcinoma(HCC),which accounts for more than 90%of primary liver cancers,is an important public health problem.In addition to cirrhosis caused by hepatitis B viral(HBV)or hepatitis C viral(HCV)infection,non-alcoholic fatty liver disease(NAFLD)is becoming a major risk factor for liver cancer because of the prevalence of obesity.Non-alcoholic steatohepatitis(NASH)will likely become the leading indication for liver transplantation in the future.It is well recognized that gut microbiota is a key environmental factor in the pathogenesis of liver disease and cancer.The interplay between gut microbiota and liver disease has been investigated in animal and clinical studies.In this article,we summarize the roles of gut microbiota in the development of liver disease as well as gut microbiota-targeted therapies. | Lijun Wang Yu-Jui Yvonne Wan | 2019 | Liver Research2019，3，1： | 12 |
| 7 | Prognosis of Hepatocellular Carcinoma: The BCLC Staging Classification显示文摘 | Josep Llovet Concepció Brú Jordi Bruix | 1999 | Semin Liver Dis1999，，03： | 11 |
| 8 | Targeting the gut barrier for the treatment of alcoholic liver disease显示文摘Alcohol consumption remains one of the predominant causes of liver disease and liver-related death worldwide.Intriguingly,dysregulation of the gut barrier is a key factor promoting the pathogenesis of alcoholic liver disease(ALD).A functional gut barrier,which consists of a mucus layer,an intact epithelial monolayer and mucosal immune cells,supports nutrient absorption and prevents bacterial penetration.Compromised gut barrier function is associated with the progression of ALD.Indeed,alcohol consumption disrupts the gut barrier,increases gut permeability,and induces bacterial translocation both in ALD patients and in experimental models with ALD.Moreover,alcohol consumption also causes enteric dysbiosis with both numerical and proportional perturbations.Here,we review and discuss mechanisms of alcohol-induced gut barrier dysfunction to better understand the contribution of the gut-liver axis to the pathogenesis of ALD.Unfortunately,there is no effectual Food and Drug Administration-approved treatment for any stage of ALD.Therefore,we conclude with a discussion of potential strategies aimed at restoring the gut barrier in ALD.The principle behind antibiotics,prebiotics,probiotics and fecal microbiota transplants is to restore microbial symbiosis and subsequently gut barrier function.Nutrientbased treatments,such as dietary supplementation with zinc,niacin or fatty acids,have been shown to regulate tight junction expression,reduce intestinal inflammation,and prevent endotoxemia as well as liver injury caused by alcohol in experimental settings.Interestingly,saturated fatty acids may also directly control the gut microbiome.In summary,clinical and experimental studies highlight the significance and efficacy of the gut barrier in treating ALD. | Zhanxiang Zhou Wei Zhong | 2017 | Liver Research2017，1，4： | 10 |
| 9 | Meta‐analysis: ARFI elastography versus transient elastography for the evaluation of liver fibrosis显示文摘 | Simona Bota Harald Herkner Ioan Sporea Petra Salzl Roxana Sirli Adriana M. Neghina Markus Peck‐Radosavljevic | 2013 | Liver Int2013，，8： | 9 |
| 10 | FOXO transcription factors in non-alcoholic fatty liver disease显示文摘Non-alcoholic fatty liver disease(NAFLD)is a chronic progressive liver disorder that begins with simple hepatic steatosis and progresses to non-alcoholic steatohepatitis,fibrosis,cirrhosis,and even liver cancer.As the global prevalence of NAFLD rises,it is increasingly important that we understand its pathogenesis and develop effective therapies for this chronic disease.Forkhead box O(FOXO)transcription factors are key downstream regulators in the insulin/insulin-like growth factor 1(IGF1)signaling pathway,and have been implicated in a range of cellular functions including the regulation of glucose,triglyceride,and cholesterol homeostasis.The role of FOXOs in the modulation of immune response and inflammation is complex,with reports of both pro-and anti-inflammatory effects.FOXOs are reported to protect against hepatic fibrosis by inhibiting proliferation and transdifferentiation of hepatic stellate cells.Mice that are deficient in hepatic FOXOs are more susceptible to non-alcoholic steatohepatitis than wild-type controls.In summary,FOXOs play a critical role in maintaining metabolic and cellular homeostasis in the liver,and dysregulation of FOXOs may be involved in the NAFLD development. | X.Charlie Dong | 2017 | Liver Research2017，1，3： | 8 |
| 11 | Modified RECIST (mRECIST) Assessment for Hepatocellular Carcinoma显示文摘 | Riccardo Lencioni Josep Llovet | 2010 | Semin Liver Dis2010，，01： | 7 |
| 12 | Heterogeneity of Patients with Intermediate (BCLC B) Hepatocellular Carcinoma: Proposal for a Subclassification to Facilitate Treatment Decisions显示文摘 | Luigi Bolondi Andrew Burroughs Jean-Fran?ois Dufour Peter Galle Vincenzo Mazzaferro Fabio Piscaglia Jean Raoul Bruno Sangro | 2012 | Semin Liver Dis2012，，04： | 7 |
| 13 | Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation显示文摘Background and aim:Overdose of acetaminophen(APAP)leads to liver injury,which is one of the most common causes of liver failure in the United States.We previously demonstrated that pharmacological activation of autophagy protects against APAP-induced liver injury in mice via removal of damaged mitochondria and APAP-adducts(APAP-ADs).Using an image-based high-throughput screening for autophagy modulators,we recently identified that chlorpromazine(CPZ),a dopamine inhibitor used for anti-schizophrenia,is a potent autophagy inducer in vitro.Therefore,the aim of the present study is to determine whether CPZ may protect against APAP-induced liver injury via inducing autophagy.Methods:Wild type C57BL/6J mice were injected with APAP to induce liver injury.CPZ was administrated either at the same time with APAP(co-treatment)or 2 h later after APAP administration(post-treat-ment).Hemotoxyline and eosin(H&E)staining of liver histology,terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling(TUNEL)staining of necrotic cell death as well as serum levels of alanine aminotransferase(ALT)were used to monitor liver injury.Results:We found that CPZ markedly protected against APAP-induced liver injury as demonstrated by decreased serum levels of ALT,liver necrotic areas as well as TUNEL-positive cells in mice that were either co-treated or post-treated with CPZ.Mechanistically,we observed that CPZ increased the number of autolysosomes and decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP.Pharmacological inhibition of autophagy by chloroquine partially weak-ened the protective effects of CPZ against APAP-induced liver injury.Conclusions:Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation. | Yuan Li Hong-Min Ni Hartmut Jaeschke Wen-Xing Ding | 2019 | Liver Research2019，3，1： | 7 |
| 14 | Alcohol and drug-induced liver injury:Metabolism,mechanisms,pathogenesis and potential therapies显示文摘The liver is one of the major metabolic organs in the body,playing a critical role in the metabolism of carbohydrates,proteins,amino acids,lipids,drugs and xenobiotics.As a result,the liver often becomes the target of drug and xenobiotics-induced damage.Currently,the most common cause for acute liver failure in the United States and multiple European countries is drug-induced liver injury(DILI).This is one of the leading causes for halting drug development and removing drugs from the consumer market. | Wen-Xing Ding Li Yang | 2019 | Liver Research2019，3，3： | 6 |
| 15 | Pyrrolizidine alkaloids:An update on their metabolism and hepatotoxicity mechanism显示文摘Pyrrolizidine alkaloids(PAs)are among the most hepatotoxic natural compounds that are widely distributed throughout the world.Most PAs are metabolically activated to trigger toxicity.Exposure to herbal medicine containing PAs and food supplements contaminated by PAs is considered to be one of the two main causes of hepatic sinusoidal obstruction syndrome(HSOS),which is a rare hepatic vascular disease with a high mortality rate.PAs-induced HSOS cases have been reported worldwide.However,there is no clinically effective therapy for PAs-induced HSOS,which is partially because the toxic mechanism is not fully understood.This review focuses on updating the information on the metabolism and the molecular mechanisms of PAs hepatotoxicity,including oxidative stress,apoptosis,and dysfunction of bile acid metabolism,and their interactions. | Jie Xu Weiqian Wang Xiao Yang Aizhen Xiong Li Yang Zhengtao Wang | 2019 | Liver Research2019，3，3： | 5 |
| 16 | Hemobilia: Etiology, diagnosis, and treatment显示文摘Hemobilia refers to bleeding from and/or into the biliary tract and is an uncommon but important cause of gastrointestinal hemorrhage.Reports of hemobilia date back to the 1600s,but due to its relative rarity and challenges in diagnosis,only in recent decades has hemobilia been more critically studied.The majority of cases of hemobilia are iatrogenic and caused by invasive procedures involving the liver,pancreas,bile ducts and/or the hepatopancreatobiliary vasculature,with trauma and malignancy rep-resenting the two other leading causes.A classic triad of right upper quadrant pain,jaundice,and overt upper gastrointestinal bleeding has been described(i.e.Quincke's triad),but this is present in only 25%e30%of patients with hemobilia.Therefore,prompt diagnosis depends critically on having a high index of suspicion,which may be based on a patient's clinical presentation and having recently undergone(peri-)biliary instrumentation or other predisposing factors.The treatment of hemobilia depends on its severity and suspected source and ranges from supportive care to advanced endoscopic,interventional radiologic,or surgical intervention.Here we provide a clinical overview and update regarding the eti-ology,diagnosis,and treatment of hemobilia geared for specialists and subspecialists alike. | Rani Berry James Han Ani A.Kardashian Nicholas F.LaRusso James H.Tabibian | 2018 | Liver Research2018，2，4： | 5 |
| 17 | Hepatic lipid homeostasis by peroxisome proliferator-activated receptor gamma 2显示文摘Peroxisome proliferator-activated receptor gamma(PPARγor PPARG)is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily.It plays a master role in the differentiation and proliferation of adipose tissues.It has two major isoforms,PPARγ1 and PPARγ2,encoded from a single gene using two separate promoters and alternative splicing.Among them,PPARγ2 is most abundantly expressed in adipocytes and plays major adipogenic and lipogenic roles in the tissue.Furthermore,it has been shown that PPARγ2 is also expressed in the liver,specifically in hepatocytes,and its expression level positively correlates with fat accumulation induced by pathological conditions such as obesity and diabetes.Knockout of the hepatic Pparg gene ameliorates hepatic steatosis induced by diet or genetic manipulations.Transcriptional activation of Pparg in the liver induces the adipogenic program to store fatty acids in lipid droplets as observed in adipocytes.Understanding how the hepatic Pparg gene expression is regulated will help develop preventative and therapeutic treatments for non-alcoholic fatty liver disease(NAFLD).Due to the potential adverse effect of hepatic Pparg gene deletion on peripheral tissue functions,therapeutic interventions that target PPAR g for fatty liver diseases require fine-tuning of this gene's expression and transcriptional activity。 | Yoon Kwang Lee Jung Eun Park Mikang Lee James P.Hardwick | 2018 | Liver Research2018，2，4： | 5 |
| 18 | Current Strategy for Staging and Treatment: The BCLC Update and Future Prospects显示文摘 | Alejandro Forner María E. Reig Carlos Rodriguez de Lope Jordi Bruix | 2010 | Semin Liver Dis2010，，01： | 5 |
| 19 | Predictive value of ALT levels for non‐alcoholic steatohepatitis ( NASH ) and advanced fibrosis in non‐alcoholic fatty liver disease ( NAFLD )显示文摘 | Siddharth Verma Donald Jensen John Hart Smruti R. Mohanty | 2013 | Liver Int2013，，9： | 5 |
| 20 | Adipose tissue autophagy and homeostasis in alcohol-induced liver injury显示文摘Alcohol consumption leads to injury in multiple organs and systems,including the liver,brain,heart,skeletal muscle,pancreas,bone,immune system,and endocrine system.Emerging evidence indicates that alcohol also promotes adipose tissue dysfunction,which may contribute to injury progression in other organs and systems.Autophagy is a lysosomal degradation pathway that has been shown to regulate adipose tissue homeostasis and adipogenesis.Increasing evidence also demonstrates that alcohol consumption affects autophagy in multiple tissues.This review summarizes current knowledge regarding the effect of autophagy on adipose tissue and its potential roles in alcohol-induced adipose tissue atrophy as well as its contribution to alcohol-induced liver injury. | Yuan Li Wen-Xing Ding | 2017 | Liver Research2017，1，1： | 5 |
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