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Status: Bibliographieeintrag

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Verfasst von:Silva, Ines [VerfasserIn]   i
 Rausch, Vanessa [VerfasserIn]   i
 Seitz, Helmut K. [VerfasserIn]   i
 Mueller, Sebastian [VerfasserIn]   i
Titel:Does Hypoxia cause carcinogenic iron accumulation in Alcoholic Liver Disease (ALD)?
Verf.angabe:Inês Silva, Vanessa Rausch, Helmut-Karl Seitz and Sebastian Mueller
E-Jahr:2017
Jahr:October 2017
Fussnoten:Gesehen am 08.04.2019
Titel Quelle:Enthalten in: Cancers
Ort Quelle:Basel : MDPI, 2009
Jahr Quelle:2017
Band/Heft Quelle:9(2017), 11, Seite 145
ISSN Quelle:2072-6694
Abstract:Alcoholic liver disease (ALD) is a leading health risk worldwide. Hepatic iron overload is frequently observed in ALD patients and it is an important and independent factor for disease progression, survival, and the development of primary liver cancer (HCC). At a systemic level, iron homeostasis is controlled by the liver-secreted hormone hepcidin. Hepcidin regulation is complex and still not completely understood. It is modulated by many pathophysiological conditions associated with ALD, such as inflammation, anemia, oxidative stress/H2O2, or hypoxia. Namely, the data on hypoxia-signaling of hepcidin are conflicting, which seems to be mainly due to interpretational limitations of in vivo data and methodological challenges. Hence, it is often overlooked that hepcidin-secreting hepatocytes are physiologically exposed to 2-7% oxygen, and that key oxygen species such as H2O2 act as signaling messengers in such a hypoxic environment. Indeed, with the recently introduced glucose oxidase/catalase (GOX/CAT) system it has been possible to independently study hypoxia and H2O2 signaling. First preliminary data indicate that hypoxia enhances H2O2-mediated induction of hepcidin, pointing towards oxidases such as NADPH oxidase 4 (NOX4). We here review and discuss novel concepts of hypoxia signaling that could help to better understand hepcidin-associated iron overload in ALD.
DOI:doi:10.3390/cancers9110145
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 ; Verlag: https://doi.org/10.3390/cancers9110145
 Volltext: https://www.mdpi.com/2072-6694/9/11/145
 DOI: https://doi.org/10.3390/cancers9110145
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:ALD
 GOX/CAT system
 HCC
 hepatic iron overload
 hepcidin
 hydrogen peroxide
 hypoxia
 NOX4
 oxidative stress
K10plus-PPN:1662945140
Verknüpfungen:→ Zeitschrift

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