Lipotoxic Hepatocyte-Derived Exosomal MicroRNA 192-5p Activates Macrophages Through Rictor/Akt/Forkhead Box Transcription Factor O1 Signaling in Nonalcoholic Fatty Liver Disease.
Identifieur interne : 000099 ( Main/Exploration ); précédent : 000098; suivant : 000100Lipotoxic Hepatocyte-Derived Exosomal MicroRNA 192-5p Activates Macrophages Through Rictor/Akt/Forkhead Box Transcription Factor O1 Signaling in Nonalcoholic Fatty Liver Disease.
Auteurs : Xiao-Lin Liu [République populaire de Chine] ; Qin Pan [République populaire de Chine] ; Hai-Xia Cao [République populaire de Chine] ; Feng-Zhi Xin [République populaire de Chine] ; Ze-Hua Zhao [République populaire de Chine] ; Rui-Xu Yang [République populaire de Chine] ; Jing Zeng [République populaire de Chine] ; Huiping Zhou [États-Unis] ; Jian-Gao Fan [République populaire de Chine]Source :
- Hepatology (Baltimore, Md.) [ 1527-3350 ] ; 2020.
Abstract
BACKGROUND AND AIMS
Hepatic macrophages can be activated by many factors such as gut-derived bacterial components and factors released from damaged hepatocytes. Macrophage polarization toward a proinflammatory phenotype (M1) represents an important event in the disease progression of nonalcoholic fatty liver disease (NAFLD). However, the underlying molecular mechanisms remain incompletely understood. Exosomes have been identified as important mediators for cell-cell communication by transferring various biological components such as microRNAs (miRs), proteins, and lipids. The role of exosomes in crosstalk between hepatocytes and macrophages in disease progression of NAFLD is yet to be explored.
APPROACH AND RESULTS
In the present study, we reported that lipotoxic injury-induced release of hepatocyte exosomes enriched with miR-192-5p played a critical role in the activation of M1 macrophages and hepatic inflammation. Serum miR-192-5p levels in patients with NAFLD positively correlated with hepatic inflammatory activity score and disease progression. Similarly, the serum miR-192-5p level and the number of M1 macrophages, as well as the expression levels of the hepatic proinflammatory mediators, were correlated with disease progression in high-fat high-cholesterol diet-fed rat models. Lipotoxic hepatocytes released more miR-192-5p-enriched exosomes than controls, which induced M1 macrophage (cluster of differentiation 11b-positive [CD11b
CONCLUSIONS
Hepatocyte-derived exosomal miR-192-5p plays a critical role in the activation of proinflammatory macrophages and disease progression of NAFLD through modulating Rictor/Akt/FoxO1 signaling. Serum exosomal miR-192-5p represents a potential noninvasive biomarker and therapeutic target for nonalcoholic steatohepatitis.
DOI: 10.1002/hep.31050
PubMed: 31782176
Affiliations:
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xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou</wicri:regionArea><wicri:noRegion>Suzhou</wicri:noRegion></affiliation></author><author><name sortKey="Pan, Qin" sort="Pan, Qin" uniqKey="Pan Q" first="Qin" last="Pan">Qin Pan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Hai Xia" sort="Cao, Hai Xia" uniqKey="Cao H" first="Hai-Xia" last="Cao">Hai-Xia Cao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Xin, Feng Zhi" sort="Xin, Feng Zhi" uniqKey="Xin F" first="Feng-Zhi" last="Xin">Feng-Zhi Xin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Ze Hua" sort="Zhao, Ze Hua" uniqKey="Zhao Z" first="Ze-Hua" last="Zhao">Ze-Hua Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Rui Xu" sort="Yang, Rui Xu" uniqKey="Yang R" first="Rui-Xu" last="Yang">Rui-Xu Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zeng, Jing" sort="Zeng, Jing" uniqKey="Zeng J" first="Jing" last="Zeng">Jing Zeng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Huiping" sort="Zhou, Huiping" uniqKey="Zhou H" first="Huiping" last="Zhou">Huiping Zhou</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:affiliation>McGuire VA Medical Center, Richmond, VA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>McGuire VA Medical Center, Richmond</wicri:cityArea></affiliation></author><author><name sortKey="Fan, Jian Gao" sort="Fan, Jian Gao" uniqKey="Fan J" first="Jian-Gao" last="Fan">Jian-Gao Fan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:31782176</idno><idno type="pmid">31782176</idno><idno type="doi">10.1002/hep.31050</idno><idno type="wicri:Area/Main/Corpus">000153</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000153</idno><idno type="wicri:Area/Main/Curation">000153</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000153</idno><idno type="wicri:Area/Main/Exploration">000153</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Lipotoxic Hepatocyte-Derived Exosomal MicroRNA 192-5p Activates Macrophages Through Rictor/Akt/Forkhead Box Transcription Factor O1 Signaling in Nonalcoholic Fatty Liver Disease.</title><author><name sortKey="Liu, Xiao Lin" sort="Liu, Xiao Lin" uniqKey="Liu X" first="Xiao-Lin" last="Liu">Xiao-Lin Liu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou</wicri:regionArea><wicri:noRegion>Suzhou</wicri:noRegion></affiliation></author><author><name sortKey="Pan, Qin" sort="Pan, Qin" uniqKey="Pan Q" first="Qin" last="Pan">Qin Pan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Hai Xia" sort="Cao, Hai Xia" uniqKey="Cao H" first="Hai-Xia" last="Cao">Hai-Xia Cao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Xin, Feng Zhi" sort="Xin, Feng Zhi" uniqKey="Xin F" first="Feng-Zhi" last="Xin">Feng-Zhi Xin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Ze Hua" sort="Zhao, Ze Hua" uniqKey="Zhao Z" first="Ze-Hua" last="Zhao">Ze-Hua Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Rui Xu" sort="Yang, Rui Xu" uniqKey="Yang R" first="Rui-Xu" last="Yang">Rui-Xu Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zeng, Jing" sort="Zeng, Jing" uniqKey="Zeng J" first="Jing" last="Zeng">Jing Zeng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Huiping" sort="Zhou, Huiping" uniqKey="Zhou H" first="Huiping" last="Zhou">Huiping Zhou</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:affiliation>McGuire VA Medical Center, Richmond, VA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>McGuire VA Medical Center, Richmond</wicri:cityArea></affiliation></author><author><name sortKey="Fan, Jian Gao" sort="Fan, Jian Gao" uniqKey="Fan J" first="Jian-Gao" last="Fan">Jian-Gao Fan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author></analytic><series><title level="j">Hepatology (Baltimore, Md.)</title><idno type="eISSN">1527-3350</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND AND AIMS</b></p><p>Hepatic macrophages can be activated by many factors such as gut-derived bacterial components and factors released from damaged hepatocytes. Macrophage polarization toward a proinflammatory phenotype (M1) represents an important event in the disease progression of nonalcoholic fatty liver disease (NAFLD). However, the underlying molecular mechanisms remain incompletely understood. Exosomes have been identified as important mediators for cell-cell communication by transferring various biological components such as microRNAs (miRs), proteins, and lipids. The role of exosomes in crosstalk between hepatocytes and macrophages in disease progression of NAFLD is yet to be explored.</p></div><div type="abstract" xml:lang="en"><p><b>APPROACH AND RESULTS</b></p><p>In the present study, we reported that lipotoxic injury-induced release of hepatocyte exosomes enriched with miR-192-5p played a critical role in the activation of M1 macrophages and hepatic inflammation. Serum miR-192-5p levels in patients with NAFLD positively correlated with hepatic inflammatory activity score and disease progression. Similarly, the serum miR-192-5p level and the number of M1 macrophages, as well as the expression levels of the hepatic proinflammatory mediators, were correlated with disease progression in high-fat high-cholesterol diet-fed rat models. Lipotoxic hepatocytes released more miR-192-5p-enriched exosomes than controls, which induced M1 macrophage (cluster of differentiation 11b-positive [CD11b</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Hepatocyte-derived exosomal miR-192-5p plays a critical role in the activation of proinflammatory macrophages and disease progression of NAFLD through modulating Rictor/Akt/FoxO1 signaling. Serum exosomal miR-192-5p represents a potential noninvasive biomarker and therapeutic target for nonalcoholic steatohepatitis.</p></div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">31782176</PMID><DateRevised><Year>2020</Year><Month>08</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1527-3350</ISSN><JournalIssue CitedMedium="Internet"><Volume>72</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Hepatology (Baltimore, Md.)</Title><ISOAbbreviation>Hepatology</ISOAbbreviation></Journal><ArticleTitle>Lipotoxic Hepatocyte-Derived Exosomal MicroRNA 192-5p Activates Macrophages Through Rictor/Akt/Forkhead Box Transcription Factor O1 Signaling in Nonalcoholic Fatty Liver Disease.</ArticleTitle><Pagination><MedlinePgn>454-469</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/hep.31050</ELocationID><Abstract><AbstractText Label="BACKGROUND AND AIMS" NlmCategory="OBJECTIVE">Hepatic macrophages can be activated by many factors such as gut-derived bacterial components and factors released from damaged hepatocytes. Macrophage polarization toward a proinflammatory phenotype (M1) represents an important event in the disease progression of nonalcoholic fatty liver disease (NAFLD). However, the underlying molecular mechanisms remain incompletely understood. Exosomes have been identified as important mediators for cell-cell communication by transferring various biological components such as microRNAs (miRs), proteins, and lipids. The role of exosomes in crosstalk between hepatocytes and macrophages in disease progression of NAFLD is yet to be explored.</AbstractText><AbstractText Label="APPROACH AND RESULTS" NlmCategory="UNASSIGNED">In the present study, we reported that lipotoxic injury-induced release of hepatocyte exosomes enriched with miR-192-5p played a critical role in the activation of M1 macrophages and hepatic inflammation. Serum miR-192-5p levels in patients with NAFLD positively correlated with hepatic inflammatory activity score and disease progression. Similarly, the serum miR-192-5p level and the number of M1 macrophages, as well as the expression levels of the hepatic proinflammatory mediators, were correlated with disease progression in high-fat high-cholesterol diet-fed rat models. Lipotoxic hepatocytes released more miR-192-5p-enriched exosomes than controls, which induced M1 macrophage (cluster of differentiation 11b-positive [CD11b<sup>+</sup> ]/CD86<sup>+</sup> ) activation and increase of inducible nitric oxide synthase, interleukin 6, and tumor necrosis factor alpha expression. Furthermore, hepatocyte-derived exosomal miR-192-5p inhibited the protein expression of the rapamycin-insensitive companion of mammalian target of rapamycin (Rictor), which further inhibited the phosphorylation levels of Akt and forkhead box transcription factor O1 (FoxO1) and resulted in activation of FoxO1 and subsequent induction of the inflammatory response.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Hepatocyte-derived exosomal miR-192-5p plays a critical role in the activation of proinflammatory macrophages and disease progression of NAFLD through modulating Rictor/Akt/FoxO1 signaling. Serum exosomal miR-192-5p represents a potential noninvasive biomarker and therapeutic target for nonalcoholic steatohepatitis.</AbstractText><CopyrightInformation>© 2019 by the American Association for the Study of Liver Diseases.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiao-Lin</ForeName><Initials>XL</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Qin</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Hai-Xia</ForeName><Initials>HX</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xin</LastName><ForeName>Feng-Zhi</ForeName><Initials>FZ</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Ze-Hua</ForeName><Initials>ZH</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Rui-Xu</ForeName><Initials>RX</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Huiping</ForeName><Initials>H</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-0050-372X</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>McGuire VA Medical Center, Richmond, VA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Jian-Gao</ForeName><Initials>JG</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>BK20190172</GrantID><Agency>Natural Science Foundation of Jiangsu Province</Agency><Country></Country></Grant><Grant><GrantID>2017YFSF090203</GrantID><Agency>National Key Research and Development Plan 'Precision Medicine Research'</Agency><Country></Country></Grant><Grant><GrantID>IS1 BX004777</GrantID><Acronym>BX</Acronym><Agency>BLRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>81470840, 81600464, 81873565, 81900508</GrantID><Agency>National Natural Science Foundation of China</Agency><Country></Country></Grant><Grant><GrantID>R01 AT004148</GrantID><Acronym>AT</Acronym><Agency>NCCIH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK115377</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>I01 BX004033</GrantID><Acronym>BX</Acronym><Agency>BLRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AA026629</GrantID><Acronym>AA</Acronym><Agency>NIAAA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>IK6 BX004477</GrantID><Acronym>BX</Acronym><Agency>BLRD VA</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK104893</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK057543</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Hepatology</MedlineTA><NlmUniqueID>8302946</NlmUniqueID><ISSNLinking>0270-9139</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>06</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31782176</ArticleId><ArticleId IdType="doi">10.1002/hep.31050</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Fan JG, Kim SU, Wong VW. 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Nat Commun 2018;9:4863.</Citation></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Virginie</li></region></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Liu, Xiao Lin" sort="Liu, Xiao Lin" uniqKey="Liu X" first="Xiao-Lin" last="Liu">Xiao-Lin Liu</name></noRegion><name sortKey="Cao, Hai Xia" sort="Cao, Hai Xia" uniqKey="Cao H" first="Hai-Xia" last="Cao">Hai-Xia Cao</name><name sortKey="Fan, Jian Gao" sort="Fan, Jian Gao" uniqKey="Fan J" first="Jian-Gao" last="Fan">Jian-Gao Fan</name><name sortKey="Fan, Jian Gao" sort="Fan, Jian Gao" uniqKey="Fan J" first="Jian-Gao" last="Fan">Jian-Gao Fan</name><name sortKey="Liu, Xiao Lin" sort="Liu, Xiao Lin" uniqKey="Liu X" first="Xiao-Lin" last="Liu">Xiao-Lin Liu</name><name sortKey="Pan, Qin" sort="Pan, Qin" uniqKey="Pan Q" first="Qin" last="Pan">Qin Pan</name><name sortKey="Xin, Feng Zhi" sort="Xin, Feng Zhi" uniqKey="Xin F" first="Feng-Zhi" last="Xin">Feng-Zhi Xin</name><name sortKey="Yang, Rui Xu" sort="Yang, Rui Xu" uniqKey="Yang R" first="Rui-Xu" last="Yang">Rui-Xu Yang</name><name sortKey="Zeng, Jing" sort="Zeng, Jing" uniqKey="Zeng J" first="Jing" last="Zeng">Jing Zeng</name><name sortKey="Zhao, Ze Hua" sort="Zhao, Ze Hua" uniqKey="Zhao Z" first="Ze-Hua" last="Zhao">Ze-Hua Zhao</name></country><country name="États-Unis"><region name="Virginie"><name sortKey="Zhou, Huiping" sort="Zhou, Huiping" uniqKey="Zhou H" first="Huiping" last="Zhou">Huiping Zhou</name></region><name sortKey="Zhou, Huiping" sort="Zhou, Huiping" uniqKey="Zhou H" first="Huiping" last="Zhou">Huiping Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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