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Mechanisms of Liver Fibrosis : = A Novel Role of Exosomes.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Mechanisms of Liver Fibrosis :/
Reminder of title:	A Novel Role of Exosomes.
Author:	Wang, Ruisi.
Description:	1 online resource (210 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 78-03, Section: B.
Contained By:	Dissertations Abstracts International78-03B.
Subject:	Biogeochemistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10141486click for full text (PQDT)
ISBN:	9781339968469

Mechanisms of Liver Fibrosis : = A Novel Role of Exosomes.
Wang, Ruisi.

Mechanisms of Liver Fibrosis :A Novel Role of Exosomes. - 1 online resource (210 pages)

Source: Dissertations Abstracts International, Volume: 78-03, Section: B.

Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2016.

Includes bibliographical references

Liver fibrosis is responsible for a disproportionate share of the cause of liver transplant and HCC. This is due to a combination of the multiple "inducers" of fibrosis, as well as the relative ineffectiveness of current therapies. We now know that hepatic stellate cells (HSCs) plays critical role in the development of liver fibrosis to therapies, as their senescence, apoptosis and inactivation are the key of treatment. Chapter 1 reviewed the recent progress of liver fibrosis, HSC research, exosome, and SK1/S1P signaling pathway and highlighted the limitations of current therapies. Chapter 2 described EC/HSC crosstalk and identified exosomes as a potential target to cure liver fibrosis. We sought to investigate whether targeting exosome endocytosis was imperative for the development of effective therapies. Chapter 3 demonstrated genetic disruption of Dyn2 GTPase activity selectively in HSCs enhanced fibrogenesis, which occurs, in part, through upregulation of the SK1/S1P pathway in HSC. Both chapters highlighted the importance of SK1/S1P pathway in HSCs. Chapter 4 discussed the exosome sorting, selective endocytosis, HSC activation, liver fibrosis treatment model, and identified future directions of the research. Toward this end, the body of work presented here elucidates a novel role of a canonical chemokine and its enzyme, S1P/SK1, as a key regulator of HSCs activation and a potential biomarker.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2023

Mode of access: World Wide Web

ISBN: 9781339968469Subjects--Topical Terms:

545717
Biogeochemistry.
Subjects--Index Terms:

DynaminIndex Terms--Genre/Form:

542853
Electronic books.

Mechanisms of Liver Fibrosis : = A Novel Role of Exosomes.
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245 1 0 $a Mechanisms of Liver Fibrosis : $b A Novel Role of Exosomes.
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500 $a Source: Dissertations Abstracts International, Volume: 78-03, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Shah, Vijay H.
502 $a Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2016.
504 $a Includes bibliographical references
520 $a Liver fibrosis is responsible for a disproportionate share of the cause of liver transplant and HCC. This is due to a combination of the multiple "inducers" of fibrosis, as well as the relative ineffectiveness of current therapies. We now know that hepatic stellate cells (HSCs) plays critical role in the development of liver fibrosis to therapies, as their senescence, apoptosis and inactivation are the key of treatment. Chapter 1 reviewed the recent progress of liver fibrosis, HSC research, exosome, and SK1/S1P signaling pathway and highlighted the limitations of current therapies. Chapter 2 described EC/HSC crosstalk and identified exosomes as a potential target to cure liver fibrosis. We sought to investigate whether targeting exosome endocytosis was imperative for the development of effective therapies. Chapter 3 demonstrated genetic disruption of Dyn2 GTPase activity selectively in HSCs enhanced fibrogenesis, which occurs, in part, through upregulation of the SK1/S1P pathway in HSC. Both chapters highlighted the importance of SK1/S1P pathway in HSCs. Chapter 4 discussed the exosome sorting, selective endocytosis, HSC activation, liver fibrosis treatment model, and identified future directions of the research. Toward this end, the body of work presented here elucidates a novel role of a canonical chemokine and its enzyme, S1P/SK1, as a key regulator of HSCs activation and a potential biomarker.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2023
538 $a Mode of access: World Wide Web
650 4 $a Biogeochemistry. $3 545717
650 4 $a Pharmaceutical sciences. $3 3173021
653 $a Dynamin
653 $a Exosome
653 $a Hepatic stellate cell
653 $a Liver fibrosis
655 7 $a Electronic books. $2 lcsh $3 542853
690 $a 0425
690 $a 0572
710 2 $a ProQuest Information and Learning Co. $3 783688
710 2 $a College of Medicine - Mayo Clinic. $b Molecular Pharmacology and Experimental Therapeutics. $3 3697704
773 0 $t Dissertations Abstracts International $g 78-03B.
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10141486 $z click for full text (PQDT)