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Perilipin 5 regulates hepatic stellate cell activation and high-fat diet-induced non-alcoholic fatty liver disease

Animal Models and Experimental Medicine 2024年第2期7卷 166-178页

作者： Xuecui Yin Lin Dong Xiaohan Wang Zhenzhen Qin Yuying Ma Xiaofei Ke Ya Li Qingde Wang Yang Mi Quanjun Lyu Xia Xu Pengyuan Zheng Youcai Tang department of Internal Medicine the Fifth Affiliated Hospital of Zhengzhou UniversityZhengzhouChina department of Pediatrics the Fifth Affiliated Hospital of Zhengzhou UniversityZhengzhouChina department of clinical Nutrition the First Affiliated Hospital of Zhengzhou UniversityZhengzhouChina Key Laboratory of Advanced drug Preparation Technologies Ministry of Education of ChinaCo-innovation Center of Henan Province for New drug R&D and Preclinical SafetySchool of Pharmaceutical SciencesZhengzhou UniversityZhengzhouChina department of Pediatrics GastroenterologyHenan Key Laboratory of Rehabilitation MedicineHenan Joint International Research Laboratory of Chronic Liver Injury and Henan Provincial Outstanding Overseas Scientists Chronic Liver Injury Studiothe Fifth Affiliated Hospital of Zhengzhou UniversityZhengzhouChina

Background:Nonalcoholic fatty liver disease(NAFLD)is one of the most common chronic liver diseases *** stellate cells(HScs)are the major effector cells of liver *** contain abundant lipid droplets(LDs)in their cytoplasm during *** 5(PLIN 5)is a LD surface-associated protein that plays a crucial role in lipid ***,little is known about the role of PLIN 5 in HSc ***:PLIN 5 was overexpressed in HScs of Sprague–Dawley rats by lentivirus *** the same time,PLIN 5 gene knockout mice were constructed and fed with a high-fat diet(HFD)for 20 weeks to study the role of PLIN 5 in *** corresponding reagent kits were used to measure TG,GSH,caspase 3 activity,ATP level,and mitochondrial DNA copy *** analysis of mice liver tissue metabolism was performed based on UPLc-MS/***,mitochondrial function,cell proliferation,and apoptosis-related genes and proteins were detected by western blotting and ***:Overexpression of PLIN 5 in activated HScs led to a decrease in ATP levels in mitochondria,inhibition of cell proliferation,and a significant increase in cell apoptosis through AMPK *** addition,compared with the HFD-fed c57BL/6J mice,PLIN 5 knockout mice fed with HFD showed reduced liver fat deposition,decreased LD abundance and size,and reduced liver ***:These findings highlight the unique regulatory role of PLIN 5 in HScs and the role of PLIN 5 in the fibrosis process of NAFLD.

关键词： AMPK apoptosis hepatic stellate cell liver fibrosis perilipin 5

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TOPK Inhibition Enhances the Sensitivity of colorectal cancer cells to Radiotherapy by Reducing the DNA Damage Response

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current Medical Science 2024年第3期44卷 545-553页

作者： Shi-gui PANG Xin ZHANG Zhao-xin LI Li-fei HE Feng cHEN Ming-long LIU Ying-ze HUANG Jian-mei MO Kong-lan LUO Juan-juan XIAO Feng ZHU department of Oncology The Affiliated Hospital of Guilin Medical UniversityGuilin541001China cancer Research Institute The Affiliated Hospital of Guilin Medical UniversityGuilin541001China Translational Medical center Huaihe HospitalHenan UniversityKaifeng475000China Guangxi Key Laboratory of Molecular Medicine in liver injury and Repair The Affiliated Hospital of Guilin Medical UniversityGuilin541001China

Objective Abnormal expression of T-lymphokine-activated killer cell-originated protein kinase(TOPK)was reported to be closely related to the resistance of prostate cancer to radiotherapy and to targeted drug resistance in lung ***,the role of TOPK inhibition in enhancing radiosensitivity of colorectal cancer(cRc)cells is *** study aimed to evaluate the radiosensitization of TOPK knockdown in cRc *** The expression of TOPK was detected in cRc tissues by immunohistochemistry,and the effect of TOPK knockdown was detected in cRc cells by Western ***-8 and clonogenic assays were used to detect the growth and clonogenic ability of cRc cells after TOPK knockdown combined with radiotherapy in cRc ***,proteomic analysis showed that the phosphorylation of TOPK downstream proteins changed after *** damage was detected by the comet *** in the DNA damage response signaling pathway were analyzed by Western blotting,and apoptosis was detected by flow *** The expression of TOPK was significantly greater in cRc tissues at grades 2–4 than in those at grade *** irradiation,cRc cells with genetically silenced TOPK had shorter comet tails and reduced expression levels of DNA damage response-associated proteins,including phospho-cyclin-dependent kinase 1(p-cDK1),phospho-ataxia telangiectasia-mutated(p-ATM),poly ADP-ribose polymerase(PARP),and meiotic recombination 11 homolog 1(MRE11).conclusions TOPK was overexpressed in patients with moderately to poorly differentiated ***,TOPK knockdown significantly enhanced the radiosensitivity of cRc cells by reducing the DNA damage response.

关键词： T-lymphokine-activated killer cell-originated protein kinase colorectal cancer DNA damage response radiosensitivity

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Precore mutation enhances viral replication to facilitate persistent infection especially in HBeAg-negative patients

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Virologica Sinica 2024年第2期39卷 319-330页

作者： Guixin Li Danli Yang Xin Liu Ting Zhang Hui Liu Jun Zou Zimeng Xu Xiangmei chen Lizhong Dai Hongsong chen Fengmin Lu Peking University People's Hospital Peking University Hepatology InstituteBeijing Key Laboratory of Hepatitis C and Immunotherapy for Liver DiseasesBeijing International Cooperation Base for Science and Technology on NAFLD DiagnosisBeijing100044China department of Microbiology and Infectious Disease center School of Basic Medical SciencesPeking UniversityBeijing100191China Baruch S.Blumberg Institute DoylestownPA18901USA Shenzhen Sanyuansheng Biotechnology co. LtdShenzhen518000China Precision Medicine center of Zhengzhou University Academy of Medical SciencesZhengzhou UniversityZhengzhou450001China Peking University-Sansure Biotech Joint Laboratory of Molecular Medicine Sansure Biotech Co.LtdChangsha410205China

Naturally occurred precore(Pc,G1896A)and/or basal core promoter(BcP,A1762T/G1764A)mutations are prevalent in chronic HBV-infected patients,especially those under HBeAg-negative ***,the replicative capacity of HBV with Pc/BcP mutations remains ***,meta-analysis showed that,only under HBeAg-negative status,the serum HBV DNA load in patients with Pc mutation was 7.41-fold higher than those without the *** Pc mutation alone and BcPþPc mutations promoted HBV replication in cell and hydrodynamic injection mouse *** human hepatocyte chimeric mouse model,BcPþPc mutations led to elevated replicative capacity and intrahepatic core protein ***,prec RNA harboring Pc mutation could serve as mRNA to express core and P proteins,and such pgRNA-like function favored the maintenance of cccDNA pool under HBeAg-negative ***,BcPþPc mutations induced more extensive and severe human hepatocyte damage as well as activated endoplasmic reticulum stress and TNF signaling pathway in livers of chimeric *** study indicates that HBeAg-negative patients should be monitored on HBV mutations regularly and are expected to receive early antiviral treatment to prevent disease progression.

关键词： hepatitis B virus Precore mutation Basal core promoter mutations Endoplasmic reticulum stress

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Transcriptomic Landscape Analysis Reveals a Persistent DNA Damage Response in Metabolic Dysfunction-associated Steatohepatitis Post-dietary Intervention

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Journal of clinical and Translational Hepatology 2024年第9期12卷 765-779页

作者： Zi-Yuan Zou Tian-Yi Ren Jia-Qi Li Ting-Ying Jiao Meng-Yu Wang Lei-Jie Huang Shuang-Zhe Lin Yuan-Yang Wang Xiao-Zhen Guo Ye-Yu Song Rui-Xu Yang cen Xie Jian-Gao Fan center for Fatty liver Department of GastroenterologyXinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina State Key Laboratory of drug Research Shanghai Institute of Materia MedicaChinese Academy of SciencesShanghaiChina University of chinese Academy of Sciences BeijingChina Human Phenome Institute School of Life SciencesFudan UniversityShanghaiChina department of Gastroenterology Ningbo No.2 HospitalNingboZhejiangChina Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition ShanghaiChina

Background and Aims:Metabolic dysfunction-associated steatotic liver disease(MASLD)and its more advanced form,metabolic dysfunction-associated steatohepatitis,have emerged as the most prevalent liver diseases ***,lifestyle modification is the foremost guidelinerecommended management strategy for ***,it remains unclear which detrimental signals persist in MASLD even after disease ***,we aimed to examine the persistent changes in liver transcriptomic profiles following this ***:Male c57BL/6J mice were divided into three groups:Western diet(WD)feeding,chow diet(cD)feeding,or diet reversal from WD to *** 16 weeks of feeding,RNA sequencing was performed on the mice’s livers to identify persistent alterations characteristic of ***,RNA sequencing databases containing high-fat diet-fed P53-knockout mice and human MASLD samples were ***:WD-induced MASLD triggered persistent activation of the DNA damage response(DDR)and its primary transcription factor,P53,long after the resolution of the hepatic phenotype through dietary *** levels of P53 might promote apoptosis,thereby exacerbating metabolic dysfunction-associated steatohepatitis,as they strongly correlated with hepatocyte ballooning,an indicator of apoptosis ***,P53 knockout in mice led to downregulated expression of apoptosis signaling in the ***,P53 may regulate apoptosis by transcriptionally activating the expression of apoptosis-enhancing nuclease(AEN).consistently,P53,AEN,and the apoptosis process all exhibited persistently elevated expression and showed a strong inter-correlation in the liver following dietary ***:The liver demonstrated upregulation of DDR signaling and the P53-AEN-apoptosis axis both during and after exposure to *** findings provide new insights into the mechanisms of MASLD relapse,highlighting DDR signaling as a promising target to prevent MASLD recu

关键词： Apoptosis DNA Damage Metabolic dysfunction-associated steatotic liver disease RNA-Seq Tumor suppressor protein P53 Western Diets

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Serum Iron Overload Activates the SMAD Pathway and Hepcidin Expression of Hepatocytes via SMURF1

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Journal of clinical and Translational Hepatology 2024年第3期12卷 227-235页

作者： Ning Zhang Pengyao Yang Yanmeng Li Qin Ouyang Fei Hou Guixin Zhu Bei Zhang Jian Huang Jidong Jia Anjian Xu Experimental and Translational Research center Beijing Friendship HospitalCapital Medical UniversityBeijingChina department of Gastroenterology Beijing Shunyi HospitalBeijingChina department of critical liver Diseases Beijing Friendship HospitalCapital Medical UniversityBeijingChina MOE Key Laboratory of Protein Science School of Life SciencesTsinghua UniversityBeijingChina liver Research center Beijing Friendship HospitalCapital Medical UniversityBeijingChina

Background and Aims:liver iron overload can induce hepatic expression of bone morphogenic protein(BMP)6 and activate the BMP/SMAD ***,serum iron overload can also activate SMAD but does not induce BMP6 ***,the mechanisms through which serum iron overload activates the BMP/SMAD pathway remain *** study aimed to clarify the role of SMURF1 in serum iron overload and the BMP/SMAD ***:A cell model of serum iron overload was established by treating hepatocytes with 2 mg/mL of holo-transferrin(Holo-Tf).A serum iron overload mouse model and a liver iron overload mouse model were established by intraperitoneally injecting 10 mg of Holo-Tf into c57BL/6 mice and administering a high-iron diet for 1 week followed by a low-iron diet for 2 *** blotting and real-time PcR were performed to evaluate the activation of the BMP/SMAD pathway and the expression of ***:Holo-Tf augmented the sensitivity and responsiveness of hepatocytes to *** E3 ubiquitin-protein ligase SMURF1 mediated Holo-Tf-induced SMAD1/5 activation and hepcidin expression;specifically,SMURF1 expression dramatically decreased when the serum iron concentration was ***,the expression of SMURF1 substrates,which are important molecules involved in the transduction of BMP/SMAD signaling,was significantly ***,in vivo analyses confirmed that SMURF1 specifically regulated the BMP/SMAD pathway during serum iron ***:SMURF1 can specifically regulate the BMP/SMAD pathway by augmenting the responsiveness of hepatocytes to BMPs during serum iron overload.

关键词： BMP/SMAD pathway Hepcidin Holo-transferrin Ubiquitin-proteasome degradation Hemochromatosis

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SRY-Box transcription factor 9 triggers YAP nuclear entry via direct interaction in tumors

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Signal Transduction and Targeted Therapy 2024年第5期9卷 2285-2297页

作者： Hui Qian chen-Hong Ding Fang Liu Shi-Jie chen chen-Kai Huang Meng-chao Xiao Xia-Lu Hong Ming-chen Wang Fang-Zhi Yan Kai Ding Ya-Lu cui Bai-Nan Zheng Jin Ding cheng Luo Xin Zhang Wei-Fen Xie department of Gastroenterology Changzheng HospitalNaval Medical UniversityShanghaiChina department of Gastroenterology Shanghai East HospitalSchool of MedicineTongji UniversityShanghaiChina drug Discovery and Design center CAS Key Laboratory of Receptor ResearchState Key Laboratory of Drug ResearchShanghai Institute of Materia MedicaChinese Academy of SciencesShanghaiChina department of Gastroenterology First Affiliated Hospital of Nanchang UniversityNanchangChina clinical cancer Institute Center for Translational MedicineNaval Medical UniversityShanghaiChina

The translocation of YAP from the cytoplasm to the nucleus is critical for its activation and plays a key role in tumor ***,the precise molecular mechanisms governing the nuclear import of YAP are not fully *** this study,we have uncovered a crucial role of SOX9 in the activation of ***9 promotes the nuclear translocation of YAP by direct ***,we have identified that the binding between Asp-125 of SOX9 and Arg-124 of YAP is essential for SOX9-YAP interaction and subsequent nuclear entry of ***,we have discovered a novel asymmetrical dimethylation of YAP at Arg-124(YAP-R124me2a)catalyzed by ***-R124me2a enhances the interaction between YAP and SOX9 and is associated with poor prognosis in multiple ***,we disrupted the interaction between SOX9 and YAP using a competitive peptide,S-A1,which mimics anα-helix of SOX9 containing Asp-125.S-A1 significantly inhibits YAP nuclear translocation and effectively suppresses tumor *** study provides the first evidence of SOX9 as a pivotal regulator driving YAP nuclear translocation and presents a potential therapeutic strategy for YAP-driven human cancers by targeting SOX9-YAP interaction.

关键词： interaction interaction precise

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clinical profile and outcomes of hepatocellular carcinoma in primary Budd-chiari syndrome

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World Journal of Gastrointestinal Oncology 2024年第3期16卷 699-715页

作者： Ankit Agarwal Sagnik Biswas Shekhar Swaroop Arnav Aggarwal Ayush Agarwal Gautam Jain Anshuman Elhence Arun Vaidya Amit Gupte Ravi Mohanka Ramesh Kumar Ashwani Kumar Mishra Shivanand Gamanagatti Shashi Bala Paul Subrat Kumar Acharya Akash Shukla Shalimar department of Gastroenterology and Human Nutrition All India Institute of Medical SciencesNew Delhi 110029DelhiIndia department of Gastroenterology Seth Gordhandas Sunderdas Medical College and KEM HospitalMumbai 400012MaharashtraIndia department of Gastroenterology Sir HN Reliance Foundation HospitalMumbai 400004India department of liver Transplant and HPB Sir HN Reliance Foundation HospitalMumbai 400004India department of Gastroenterology All India Institute of Medical SciencesPatna 801507India Professor of Biostatistics National Drug Dependence Treatment Centre(NDDTC)All India Institute of Medical SciencesNew Delhi 110029India department of Radiodiagnosis All India Institute of Medical SciencesNew Delhi 110029DelhiIndia

BAcKGROUND There is scant literature on hepatocellular carcinoma(Hcc)in patients with Budd-chiari syndrome(BcS).AIM To assess the magnitude,clinical characteristics,feasibility,and outcomes of treatment in *** A total of 904 BcS patients from New Delhi,India and 1140 from Mumbai,India were *** prevalence and incidence of Hcc were determined,and among patients with BcS-Hcc,the viability and outcomes of interventional therapy were *** In the New Delhi cohort of 35 BcS-Hcc patients,18 had Hcc at index presentation(prevalence 1.99%),and 17 developed Hcc over a follow-up of 4601 person-years,[incidence 0.36(0.22-0.57)per 100 person-years].BcS-Hcc patients were older when compared to patients with BcS alone(P=0.001)and had a higher proportion of inferior vena cava block,cirrhosis,and long-segment vascular *** median alpha-fetoprotein level was higher in patients with BcS-Hcc at first presentation than those who developed Hcc at follow-up(13029 ng/mL vs 500 ng/mL,P=0.01).Of the 35 BcS-Hcc,26(74.3%)underwent radiological interventions for BcS,and 22(62.8%)patients underwent treatment for Hcc[transarterial chemoembolization in 18(81.8%),oral tyrosine kinase inhibitor in 3(13.6%),and transarterial radioembolization in 1(4.5%)].The median survival among patients who underwent interventions for Hcc compared with those who did not was 3.5 years vs 3.1 mo(P=0.0001).In contrast to the New Delhi cohort,the Mumbai cohort of BcS-Hcc patients were predominantly males,presented with a more advanced Hcc[Barcelona clinic liver cancer c and D],and 2 patients underwent liver *** Hcc is not uncommon in patients with *** interventions and liver transplantation are feasible in select primary BcS-Hcc patients and may improve outcomes.

关键词： Budd chiari syndrome cancer cirrhosis Thrombosis liver Varices Transarterial chemoembolization Hepatic venous outflow tract obstruction

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Overview on acute-on-chronic liver failure

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Frontiers of Medicine 2016年第1期10卷 1-17页

作者： Jing Zhang Shan Gao Zhongping Duan Ke-Qin Hu department of hepatitis c and drug induced liver injury Beijing YouAn Hospital Capital Medical University Beij'ing 100069 China Beijing Artificial liver Treatment & Training center Beijing YouAn Hospital Capital Medical University~ Be~'ng 100069 Chinai' collaborative Innovation center of lnfectious Diseases Beijing 100069 China Division of Gastroenterology and Hepatology University of California Irvine Medical Center Orange CA 92868 USA

liver failure （LF） is defined as severe dysfunction in hepatic synthesis, detoxification, and metabolism induced by various etiologies. cHnical presentation of LF typically includes severe jaundice, coagulation disorder, hepatic encephalopathy, and ascites. LF can be classified into acute LF, acute-on-chronic LF （AcLF）, and chronic LF. AcLF has been demonstrated as a distinct syndrome with unique clinical presentation and outcomes. The severity, curability, and reversibility of AcLF have attracted considerable attention. Remarkable developments in AcLF-related conception, diagnostic criteria, pathogenesis, and therapy have been achieved. However, this disease, especially its diagnostic criteria, remains controversial. In this paper, we systemically reviewed the current understanding of AcLF from its definition, etiology, pathophysiology, pathology, and clinical presentation to management by thoroughly comparing important findings between east and west countries, as well as those from other regions. We also discussed the controversies, challenges, and needs for future studies to promote the standardization and optimization of the diagnosis and treatment for AcLF.

关键词： liver failure chronic liver failure acute-on-chronic liver failure diagnosis prognosis treatment

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ccL9/ccR1 axis-driven chemotactic nanovesicles for attenuating metastasis of SMAD4-deficient colorectal cancer by trapping TGF-β

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Acta Pharmaceutica Sinica B 2024年第8期14卷 3711-3729页

作者： Boning Niu Tianyi Tian Lu Wang Yinmei Tian Tian Tian Yuanyuan Guo Hu Zhou Zhiping Zhang Tongji School of Pharmacy Huazhong University of Science and TechnologyWuhan 430030China department of Oncology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China department of Pharmacy Liyuan HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China School of Pharmaceutical Sciences Fujian Provincial Key Laboratory of Innovative Drug Target ResearchHigh Throughput Drug Screening PlatformXiamen UniversityXiamen 361102China National Engineering Research center for Nanomedicine Huazhong University of Science and TechnologyWuhan 430030China Hubei Engineering Research centre for Novel drug Delivery System Huazhong University of Science and TechnologyWuhan 430030China

SMAD4 deficiency in colorectal cancer(cRc)is highly correlated with liver metastasis and high mortality,yet there are few effective precision therapies ***,we show that ccR1^(+)-granulocytic myeloid-derived suppressor cells(G-MDScs)are highly infiltrated in SMAD4-deficient cRc via ccL15/ccR1 and ccL9/ccR1 axis in clinical specimens and mouse models,*** excessive TGF-β,secreted by tumor-infiltrated ccR1^(+)-G-MDScs,suppresses the immune response of cytotoxic T lymphocytes(cTLs),thus facilitating ***,we develop engineered nanovesicles displaying ccR1 and TGFBR2 molecules(c/T-NVs)to chemotactically target the tumor driven by ccL9/ccR1 axis and trap TGF-βthrough TGF-β-TGFBR2 specific *** c/T-NVs counteract ccR1^(+)-G-MDSc infiltration through competitive responding ccL9/ccR1 axis.c/T-NVs-induced intratumoral TGF-βexhaustion alleviates the TGF-β-suppressed immune response of ***,c/T-NVs attenuate liver metastasis of SMAD4-deficient *** further exploration,high expression of programmed cell death ligand-1(PD-L1)is observed in clinical specimens of SMAD4-deficient *** c/T-NVs with anti-PD-L1 antibody(aPD-L1)induces tertiary lymphoid structure formation with sustained activation of cTLs,cXcL13^(+)-cD4^(+)T,cXcR5^(+)-cD20^(+)B cells,and enhanced secretion of cytotoxic cytokine interleukin-21 and IFN-γaround tumors,thus eradicating metastatic *** strategy elicits pleiotropic antimetastatic immunity,paving the way for nanovesicle-mediated precision immunotherapy in SMAD4-deficient cRc.

关键词： SMAD4-deficient cRc Metastasis G-MDScs TGF-β ccR1 TGFBR2

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Fenofibrate-promoted hepatomegaly and liver regeneration are PPARα-dependent and partially related to the YAP pathway

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Acta Pharmaceutica Sinica B 2024年第7期14卷 2992-3008页

作者： Shicheng Fan Yue Gao Pengfei Zhao Guomin Xie Yanying Zhou Xiao Yang Xuan Li Shuaishuai Zhang Frank JGonzalez Aijuan Qu Min Huangb Huichang Bi NMPA Key Laboratory for Research and Evaluation of drug Metabolism&Guangdong Provincial Key Laboratory of New drug Screening&Guangdong-Hongkong-Macao Joint Laboratory for New drug Screening School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China Guangdong Provincial Key Laboratory of New drug Design and Evaluation School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China department of Physiology and Pathophysiology School of Basic Medical SciencesCapital Medical UniversityBeijing 100069China Laboratory of Metabolism Center for Cancer ResearchNational Cancer InstituteNational Institutes of HealthBethesdaMD 20892USA The State Key Laboratory of chemical Oncogenomics School of Chemical Biology and BiotechnologyShenzhen Graduate School of Peking UniversityShenzhen 518055China

Fenofibrate,a peroxisome proliferator-activated receptor α(PPARα)agonist,is widely prescribed for hyperlipidemia *** studies also showed that it has therapeutic potential in various liver ***,its effects on hepatomegaly and liver regeneration and the involved mechanisms remain ***,the study showed that fenofibrate significantly promoted liver enlargement and regeneration post-partial hepatectomy in mice,which was dependent on hepatocyteexpressed PPARα.Yes-associated protein(YAP)is pivotal in manipulating liver growth and *** further identified that fenofibrate activated YAP signaling by suppressing its K48-linked ubiquitination,promoting its K63-linked ubiquitination,and enhancing the interaction and transcriptional activity of the YAP-TEAD *** inhibition of YAP-TEAD interaction using verteporfin or suppression of YAP using AAV Yap shRNA in mice significantly attenuated fenofibrate-induced *** factors,such as MYc,KRT23,RAS,and RHOA,might also participate in fenofibrate-promoted hepatomegaly and liver *** studies demonstrate that fenofibratepromoted liver enlargement and regeneration are PPARα-dependent and partially through activating the YAP signaling,with clinical implications of fenofibrate as a novel therapeutic agent for promoting liver regeneration.

关键词： Fenofibrate PPARa Hepatomegaly Partial hepatectomy liver regeneration YAP TEAD Ubiquitination

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