Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Jung, Yoon-Seok [VerfasserIn]   i
 Radhakrishnan, Kamalakannan [VerfasserIn]   i
 Hammad, Seddik [VerfasserIn]   i
 Mueller, Sebastian [VerfasserIn]   i
 Müller, Johannes [VerfasserIn]   i
 Noh, Jung-Ran [VerfasserIn]   i
 Kim, Jina [VerfasserIn]   i
 Lee, In-Kyu [VerfasserIn]   i
 Cho, Sung Jin [VerfasserIn]   i
 Kim, Don-Kyu [VerfasserIn]   i
 Kim, Yong-Hoon [VerfasserIn]   i
 Lee, Chul-Ho [VerfasserIn]   i
 Dooley, Steven [VerfasserIn]   i
 Choi, Hueng-Sik [VerfasserIn]   i
Titel:ERRγ-inducible FGF23 promotes alcoholic liver injury through enhancing CYP2E1 mediated hepatic oxidative stress
Verf.angabe:Yoon Seok Jung, Kamalakannan Radhakrishnan, Seddik Hammad, Sebastian Müller, Johannes Müller, Jung-Ran Noh, Jina kim, In-Kyu Lee, Sung Jin Cho, Don-Kyu Kim, Yong-Hoon Kim, Chul-Ho Lee, Steven Dooley, Hueng-Sik Choi
E-Jahr:2024
Jahr:May 2024
Umfang:12 S.
Fussnoten:Online veröffentlicht: 5. März 2024 ; Gesehen am 25.11.2024
Titel Quelle:Enthalten in: Redox Biology
Ort Quelle:Amsterdam [u.a.] : Elsevier, 2013
Jahr Quelle:2024
Band/Heft Quelle:71(2024), Artikel-ID 103107, Seite 103107-1-103107-12
ISSN Quelle:2213-2317
Abstract:Fibroblast growth factor 23 (FGF23) is a member of endocrine FGF family, along with FGF15/19 and FGF21. Recent reports showed that under pathological conditions, liver produces FGF23, although the role of hepatic FGF23 remains nebulous. Here, we investigated the role of hepatic FGF23 in alcoholic liver disease (ALD) and delineated the underlying molecular mechanism. FGF23 expression was compared in livers from alcoholic hepatitis patients and healthy controls. The role of FGF23 was examined in hepatocyte-specific knock-out (LKO) mice of cannabinoid receptor type 1 (CB1R), estrogen related receptor γ (ERRγ), or FGF23. Animals were fed with an alcohol-containing liquid diet alone or in combination with ERRγ inverse agonist. FGF23 is mainly expressed in hepatocytes in the human liver, and it is upregulated in ALD patients. In mice, chronic alcohol feeding leads to liver damage and induced FGF23 in liver, but not in other organs. FGF23 is transcriptionally regulated by ERRγ in response to alcohol-mediated activation of the CB1R. Alcohol induced upregulation of hepatic FGF23 and plasma FGF23 levels is lost in ERRγ-LKO mice, and an inverse agonist mediated inhibition of ERRγ transactivation significantly improved alcoholic liver damage. Moreover, hepatic CYP2E1 induction in response to alcohol is FGF23 dependent. In line, FGF23-LKO mice display decreased hepatic CYP2E1 expression and improved ALD through reduced hepatocyte apoptosis and oxidative stress. We recognized CBIR-ERRγ-FGF23 axis in facilitating ALD pathology through hepatic CYP2E1 induction. Thus, we propose FGF23 as a potential therapeutic target to treat ALD.
DOI:doi:10.1016/j.redox.2024.103107
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1016/j.redox.2024.103107
 Volltext: https://www.sciencedirect.com/science/article/pii/S2213231724000831
 DOI: https://doi.org/10.1016/j.redox.2024.103107
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Alcoholic liver disease
 CYP2E1
 ERRγ
 FGF23
 Oxidative stress
K10plus-PPN:1909428655
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/69276216   QR-Code
zum Seitenanfang