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Liver-adipose tissue crosstalk in alcohol-associated liver disease: The role of mTOR

Liver Research 2022年第4期6卷 227-237页

作者： Yssa Rodriguez Jack Dunfield Tyson Roderique hong-min ni Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA

Background:Alcohol-associated liver disease(ALD)is a major chronic liver disease around the world without successful *** alcoholic hepatitis is one of the most severe forms of ALD with high mortality,which is often associated with binge *** drinking dysregulates lipid metabolism,increases adipose tissue lipolysis,and induces liver steatosis and adipose tissue *** ev-idence implicates that crosstalk of liver and adipose tissue in the pathogenesis of *** target of rapamycin(mTOR)is a phosphatidylinositol 3-kinase(PI3K)-like serine/threonine protein kinase that regulates lipid metabolism,cell proliferation and ***,the role of mTOR in regulating adipose-liver crosstalk in binge drinking-induced organ damage remains ***:We generated liver-specific and adipocyte-specific regulatory-associated protein of mTOR(Rptor)knockout(Rptor LKO and Rptor AKO)as well as Mtor knockout(Mtor LKO and Mtor AKO)mice,by crossing Rptor flox and Mtor flox mice with albumin Cre or adiponectin Cre mice,*** addition,we generated liver and adipocyte double deletion of Rptor or Mtor(Mtor LAKO and Rptor LAKO)*** knockout mice with their matched wild-type littermates(Rptor WT and Mtor WT)were subjected to acute gavage of 7 g/kg ***:Mice with adipocyte deletion of Rptor or Mtor developed hepatomegaly and adipose tissue *** gavage increased liver injury,hepatic steatosis and inflammation in mouse livers as demonstrated by elevated serum alanine aminotransferase activities,increased hepatic levels of tri-glyceride and increased hepatic numbers of CD68 positive macrophages in mouse livers after alcohol *** injury was further exacerbated by deletion of adipocyte Rptor or *** adipokine array analysis revealed that increased levels of pro-inflammatory cytokines IL-6 and TNF a as well as chemokine MCP-1 following acute alcohol gavage in wild-type mice,which were further incr

关键词： Alcohol-associated liver disease(ALD) Liver injury Mechanistic target of rapamycin(mTOR) Adipose atrophy Adipokine Liver-adipose tissue crosstalk

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Necroptosis in ischemia-reperfusion injury of lean and steatotic livers

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Liver Research 2019年第3期3卷 227-233页

作者： Hua Sun Tara McKeen Hua Wang hong-min ni Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA Department of Oncology The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhuiChina

Hepatic ischemia-reperfusion(IR)injury is a major complication during liver transplantation,liver resection,and other clinical *** hepatic IR injury in steatotic livers is a major reason for rejecting the use of steatotic livers for liver *** is implicated in the pathogenesis of fatty liver diseases,including non-alcoholic fatty liver disease(NAFLD)and alcoholic liver disease(ALD).Necroptosis is one type of regulated cell death and is regulated by three key proteins:receptorinteracting protein 1(RIP1),receptor-interacting protein 3(RIP3),and mixed-lineage kinase domainlike protein(MLKL).In this review,we examine the necroptosis status in the steatotic liver diseases NAFLD and ALD as well as its role in hepatic IR injury of lean and steatotic livers.

关键词： Necroptosis Non-alcoholic fatty liver disease(NAFLD) Alcoholic liver disease(ALD) Ischemia-reperfusion(IR) Liver injury

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Loss of hepatic VMP1 trapped VLDL in the bilayer of endoplasmic reticulum membrane

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Liver Research 2023年第2期7卷 161-163页

作者： hong-min ni Benjamin Ding Allen Chen Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA

Non-alcoholic fatty liver disease(NAFLD)is a highly prevalent form of liver disease associated with obesity,diabetes,and other metabolic diseases.1 NAFLD is characterized by hepatocyte lipid *** untreated,this disease can progress to nonalcoholic steatohepatitis(NASH),typified by increased hepatocyte death,hepatocyte ballooning,inflammation,and fibrosis.2,3 The molecular basis of NAFLD/NASH development and progression is still poorly understood;thus,no effective treatments currently exist to combat this burgeoning health problem.

关键词： Autophagy Lipid droplet Non-alcoholic fatty liver disease(NAFLD) Non-alcoholic steatohepatitis(NASH)

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Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation

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Liver Research 2019年第1期3卷 65-74页

作者： Yuan Li hong-min ni Hartmut Jaeschke Wen-Xing Ding Department of Pharmacology Toxicology and TherapeuticsThe University of Kansas Medical CenterKansas CityKSUSA

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 *** 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 ***,the aim of the present study is to determine whether CPZ may protect against APAP-induced liver injury via inducing ***:Wild type C57BL/6J mice were injected with APAP to induce liver *** 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 ***: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 ***,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 *** inhibition of autophagy by chloroquine partially weak-ened the protective effects of CPZ against APAP-induced liver ***:Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation.

关键词： Chlorpromazine(CPZ) Acetaminophen(APAP) Drug-induced liver injury Necrosis Autolysosome Hepatotoxicity Glutathione(GSH) Oxidant stress

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Dual roles of p62/SQSTM1 in the injury and recovery phases of acetaminophen-induced liver injury in mice

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Acta Pharmaceutica Sinica B 2021年第12期11卷 3791-3805页

作者： Hui Qian Qingyun Bai Xiao Yang Jephte Y.Akakpo Lili Ji Li Yang Thomas Rulicke Kurt Zatloukal Hartmut Jaeschke hong-min ni Wen-Xing Ding Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKS 66160USA The MOE Key Laboratory for Standardization of Chinese Medicines Shanghai Key Laboratory of Compound Chinese Medicines and the SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese MedicinesInstitute of Chinese Materia MedicaShanghai University of Traditional Chinese MedicineShanghai 201203China School of Chemistry and Bioengineering Yichun UniversityYichun 336000China Department of Biomedical Sciences University of Veterinary Medicine Vienna Veterina¨rplatzVienna 1210Austria The Institute of Pathology Medical University of GrazGraz A-8036Austria

Acetaminophen(APAP)overdose can induce liver injury and is the most frequent cause of acute liver failure in the United *** investigated the role of p62/SQSTM1(referred to as p62)in APAP-induced liver injury(AILI)in *** found that the hepatic protein levels of p62 dramatically increased at 24 h after APAP treatment,which was inversely correlated with the hepatic levels of *** also activated mTOR at 24 h,which is associated with increased cell *** contrast,p62 knockout(KO)mice showed increased hepatic levels of APAP-adducts detected by a specific antibody using Western blot analysis but decreased mTOR activation and cell proliferation with aggravated liver injury at 24 h after APAP ***,p62 KO mice recovered from AILI whereas the wild-type mice still sustained liver injury at 48 *** found increased number of infiltrated macrophages in p62 KO mice that were accompanied with decreased hepatic von Willebrand factor(VWF)and platelet aggregation,which are associated with increased cell proliferation and improved liver injury at 48 h after APAP *** data indicate that p62 inhibits the late injury phase of AILI by increasing autophagic selective removal of APAP-adducts and mitochondria but impairs the recovery phase of AILI likely by enhancing hepatic blood coagulation.

关键词： Autophagy Coagulation DILI Liver regeneration Macrophage Hepatotoxicity Platelet

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Liver-specific deletion of mechanistic target of rapamycin does not protect against acetaminophen-induced liver injury in mice

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Liver Research 2021年第2期5卷 79-87页

作者： Hua Sun hong-min ni Jennifer M.McCracken Jephte Y Akakpo Sam Fulte Tara McKeen Hartmut Jaeschke Hua Wang Wen-Xing Ding Department of Pharmacology Toxicology and TherapeuticsThe University of Kansas Medical CenterKansas CityKSUSA Department of Oncology The First Affiliated Hospital of Anhui Medical UniversityHefeiChina

Background:Acetaminophen(APAP)overdose can cause liver injury and liver failure,which is one of the most common causes of drug-induced liver injury in the United *** activation of autophagy by inhibiting mechanistic target of rapamycin(mTOR)protects against APAP-induced liver injury likely via autophagic removal of APAP-adducts and damaged *** the present study,we aimed to investigate the role of genetic ablation of mTOR pathways in mouse liver in APAP-induced liver injury and liver repair/***:Albumin-Cre(Alb-Cre)mice,mTOR^(f/f) and Raptor^(f/f) mice(C57BL/6J background)were crossbred to produce liver-specific mTOR knockout(L-mTOR KO,Alb Cret/-,mTOR^(f/f))and liver-specific Raptor KO(L-Raptor,Alb Cret/-,Raptor^(f/f))***-Cre littermates were used as wild-type(WT)*** mice were treated with APAP for various time points for up to 48 *** injury,cell proliferation,autophagy and mTOR activation were ***:We found that genetic deletion of neither Raptor,an important adaptor protein in mTOR complex 1,nor mTOR,in the mouse liver significantly protected against APAP-induced liver injury despite increased hepatic autophagic *** deletion of Raptor or mTOR in mouse livers did not affect APAP metabolism and APAP-induced c-Jun N-terminal kinase(JNK)activation,but slightly improved mouse survival likely due to increased hepatocyte ***:Our results indicate that genetic ablation of mTOR in mouse livers does not protect against APAP-induced liver injury but may slightly improve liver regeneration and mouse survival after APAP overdose.

关键词： Acetaminophen(APAP) Autophagy Hepatotoxicity Liver injury Liver regeneration Mechanistic target of rapamycin(mTOR) Regulatory associated protein of mTOR complex(Raptor)

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High-throughput screening of novel TFEB agonists in protecting against acetaminopheninduced liver injury in mice

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Acta Pharmaceutica Sinica B 2024年第1期14卷 190-206页

作者： Xiaojuan Chao Mengwei niu Shaogui Wang Xiaowen Ma Xiao Yang Hua Sun Xujia Hu Hua Wang Li Zhang Ruili Huang Menghang Xia Andrea Ballabio Hartmut Jaeschke hong-min ni Wen-Xing Ding Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKS 66160USA NMPA Key Laboratory for Research and Evaluation of Drug Metabolism&Guangdong Provincial Key Laboratory of New Drug Screening School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China Department of Oncology the First Affiliated Hospital of Anhui Medical UniversityAnhui Medical UniversityHefei 230032China National Center for Advancing Translational Sciences National Institutes of HealthBethesdaMD 20892USA Telethon Institute of Genetics and Medicine TIGEMPozzuoliNaples 80131Italy Medical Genetics Department of Translational MedicineFederico II UniversityNaples 80131Italy Department of Molecular and Human Genetics Baylor College of MedicineHoustonTX 77030USA Department of Internal Medicine Division of GastroenterologyHepatology&MotilityUniversity of Kansas Medical CenterKansas CityKS 66160USA

Macroautophagy(referred to as autophagy hereafter)is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and *** studies showed that autophagy protects against acetaminophen(APAP)-induced injury(AILI)via selective removal of damaged mitochondria and APAP protein *** lysosome is a critical organelle sitting at the end stage of autophagy for autophagic degradation via fusion with *** the present study,we showed that transcription factor EB(TFEB),a master transcription factor for lysosomal biogenesis,was impaired by APAP resulting in decreased lysosomal biogenesis in mouse *** loss-of and gain-of function of hepatic TFEB exacerbated or protected against AILI,***,overexpression of TFEB increased clearance of APAP protein adducts and mitochondria biogenesis as well as SQSTM1/p62-dependent non-canonical nuclear factor erythroid 2-related factor 2(NRF2)activation to protect against *** also performed an unbiased cell-based imaging high-throughput chemical screening on TFEB and identified a group of TFEB *** these agonists,salinomycin,an anticoccidial and antibacterial agent,activated TFEB and protected against AILI in *** conclusion,genetic and pharmacological activating TFEB may be a promising approach for protecting against AILI.

关键词： Autophagy DILI Drug screening Hepatotoxicity Lysosome Mitochondria Mitophagy NRF2

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Pink1/Parkin双敲除小鼠缺乏线粒体自噬加重对乙酰氨基酚诱发的肝脏损伤（英文）

Pink1/Parkin双敲除小鼠缺乏线粒体自噬加重对乙酰氨基酚诱发的肝...

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2017环境与公共健康学术会议暨中国环境科学学会环境医学与健康分会、中国毒理学会生化与分子毒理专业委员会2017年年会

作者： Hua Wang hong-min ni Wen-Xing Ding Department of Toxicology School of Public HealthAnhui Medical University Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical Center

Background/Aim:Increasing studies report that Pink1-Parkin pathway plays a crucial role in modulating mitophagy in mammalian *** previous study found that mitophagy still occurred in APAP-treated livers of Parkin knockout(KO) mice,and less liver injury was observed in APAP-administered Parkin KO mice as compared to wild type(WT) ***,such compensatory pathways responsible for Parkin-independent mitophagy have not been ***

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基于网络外部性的企业横向兼并研究

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系统工程学报 2003年第2期18卷 109-114页

作者：翁轶丛陈宏民倪苏云上海交通大学管理学院上海200030

利用三阶段动态博弈模型,研究了存在4家企业、具有网络外部性特征的市场中,企业横向兼并的动机及社会效应.研究表明,即使面临跟随厂商进行兼并反击的威胁,先动厂商始终具有兼并动机,而跟随厂商的反击策略与网络外部性的强度有关.在均衡... 详细信息

利用三阶段动态博弈模型,研究了存在4家企业、具有网络外部性特征的市场中,企业横向兼并的动机及社会效应.研究表明,即使面临跟随厂商进行兼并反击的威胁,先动厂商始终具有兼并动机,而跟随厂商的反击策略与网络外部性的强度有关.在均衡状态下,尽管当网络外部性强度处于一定范围时,消费者剩余会受到损害,但是社会福利将得到改善.

关键词：企业兼并网络外部性博弈论计算机网络

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Theoretical and Experimental Study of A Coaxial Double-Buoy Wave Energy Converter

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China Ocean Engineering 2021年第3期35卷 454-464页

作者： LI De-min DONG Xiao-chen SHI hong-da LI Yan-ni Department of Ocean Engineering College of EngineeringOcean University of ChinaQingdao 266100China Shandong Provincial Key Laboratory of Ocean Engineering Ocean University of ChinaQingdao 266100China Qingdao Municipal Key Laboratory of Ocean Renewable Energy Ocean University of ChinaQingdao 266100China Pilot National Laboratory for Marine Science and Technology(QingDao) Qingdao 266200China

The double-body heave wave energy converter(WEC)is one of the most conducive devices to absorb the wave energy from relative motion while the law of which is not well *** paper makes an in-depth study on this wave energy converter,by means of the combination of theoretical analysis and physical model *** hydrodynamic characteristics and energy capture of the double-buoy under constant and linear Power Take-Off(PTO)damping are *** of absolute mass and mass ratio are discussed in the theoretical *** displacement amplitude and average power output are tested in the experiment to analyze the effect of the wave period and outer buoy’s mass,while the capture width ratio(CWR)is also *** show that the wave period and mass of the buoys have a significant effect on the *** forms of PTO damping have no influence on the optimal wave period and mass ratio of this *** is recommended to select the double-buoy converter with a mass ratio of 0.80 and to place it in an area with the frequent wave period close to the natural period of the outer buoy to achieve the optimal energy capture.

关键词： coaxial double-buoy wave energy converter hydrodynamic characteristics model test power take-off

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