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

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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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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维普期刊数据库

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Editorial of special column on Drug targets and drug development for Alzheimer's disease

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Acta Pharmaceutica Sinica B 2022年第4期12卷 1686-1687页

作者： Wen-Xing Ding russell H.Swerdlow Department of Pharmacology Toxicology and TherapeuticsDepartment of Internal Medicinethe University of Kansas Medical CenterKansas CityKS 66160USA Department of Neurology the University of Kansas Medical CenterKansas CityKS 66160USA

Alzheimer's disease(AD)is the most common form of progressive dementia in people aged 65 years and *** major pathological features of AD are the accumulation of extracellularβ-amyloid plaques and intracellular neurofibrillary tangles composed of aggregated,hyperphosphorylated *** addition to an accumulation of protein aggregates,mitochondrial dysfunction,altered lipid metabolism and increased neuroinflammation also play critical roles in the pathogenesis of AD and its associated dementia.

关键词： Alzheimer metabolism inflammation

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