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Status: Bibliographieeintrag

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Verfasst von:Neuman, Manuela G. [VerfasserIn]   i
 Seitz, Helmut K. [VerfasserIn]   i
 French, Samuel W. [VerfasserIn]   i
 Malnick, Stephen [VerfasserIn]   i
 Tsukamoto, Heidekazu [VerfasserIn]   i
 Cohen, Lawrence B. [VerfasserIn]   i
 Hoffman, Paula [VerfasserIn]   i
 Tabakoff, Boris [VerfasserIn]   i
 Fasullo, Michael [VerfasserIn]   i
 Nagy, Laura E. [VerfasserIn]   i
 Tuma, Pamela L. [VerfasserIn]   i
 Schnabl, Bernd [VerfasserIn]   i
 Mueller, Sebastian [VerfasserIn]   i
 Groebner, Jennifer L. [VerfasserIn]   i
 Barbara, French A. [VerfasserIn]   i
 Yue, Jia [VerfasserIn]   i
 Nikko, Afifiyan [VerfasserIn]   i
 Alejandro, Mendoza [VerfasserIn]   i
 Brittany, Tillman [VerfasserIn]   i
 Edward, Vitocruz [VerfasserIn]   i
 Harrall, Kylie [VerfasserIn]   i
 Saba, Laura [VerfasserIn]   i
 Mihai, Opris [VerfasserIn]   i
Titel:Alcoholic-hepatitis, links to brain and microbiome
Titelzusatz:mechanisms, clinical and experimental research
Verf.angabe:Manuela G. Neuman, Helmut Karl Seitz, Samuel W. French, Stephen Malnick, Heidekazu Tsukamoto, Lawrence B. Cohen, Paula Hoffman, Boris Tabakoff, Michael Fasullo, Laura E. Nagy, Pamela L. Tuma, Bernd Schnabl, Sebastian Mueller, Jennifer L. Groebner, French A. Barbara, Jia Yue, Afifiyan Nikko, Mendoza Alejandro, Tillman Brittany, Vitocruz Edward, Kylie Harrall, Laura Saba and Opris Mihai
E-Jahr:2020
Jahr:18 March 2020
Fussnoten:Gesehen am 17.06.2020
Titel Quelle:Enthalten in: Biomedicines
Ort Quelle:Basel : MDPI, 2013
Jahr Quelle:2020
Band/Heft Quelle:8(2020,3) Artikel-Nummer 63, 28 Seiten
ISSN Quelle:2227-9059
Abstract:The following review article presents clinical and experimental features of alcohol-induced liver disease (ALD). Basic aspects of alcohol metabolism leading to the development of liver hepatotoxicity are discussed. ALD includes fatty liver, acute alcoholic hepatitis with or without liver failure, alcoholic steatohepatitis (ASH) leading to fibrosis and cirrhosis, and hepatocellular cancer (HCC). ALD is fully attributable to alcohol consumption. However, only 10–20% of heavy drinkers (persons consuming more than 40 g of ethanol/day) develop clinical ALD. Moreover, there is a link between behaviour and environmental factors that determine the amount of alcohol misuse and their liver disease. The range of clinical presentation varies from reversible alcoholic hepatic steatosis to cirrhosis, hepatic failure, and hepatocellular carcinoma. We aimed to (1) describe the clinico-pathology of ALD, (2) examine the role of immune responses in the development of alcoholic hepatitis (ASH), (3) propose diagnostic markers of ASH, (4) analyze the experimental models of ALD, (5) study the role of alcohol in changing the microbiota, and (6) articulate how findings in the liver and/or intestine influence the brain (and/or vice versa) on ASH; (7) identify pathways in alcohol-induced organ damage and (8) to target new innovative experimental concepts modeling the experimental approaches. The present review includes evidence recognizing the key toxic role of alcohol in ALD severity. Cytochrome p450 CYP2E1 activation may change the severity of ASH. The microbiota is a key element in immune responses, being an inducer of proinflammatory T helper 17 cells and regulatory T cells in the intestine. Alcohol consumption changes the intestinal microbiota and influences liver steatosis and liver inflammation. Knowing how to exploit the microbiome to modulate the immune system might lead to a new form of personalized medicine in ALF and ASH.
DOI:doi:10.3390/biomedicines8030063
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/biomedicines8030063
 Volltext: https://www.mdpi.com/2227-9059/8/3/63
 DOI: https://doi.org/10.3390/biomedicines8030063
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:acetaldehyde dehydrogenase (ALDH)
 alcohol dehydrogenase (ADH)
 alcoholic hepatitis
 CYP 1A1
 CYP 1A2
 CYP2E1
 hepato-carcinogenesis
 hepatocytotoxicity
 his3-Δ3′ and his3<i>-</i> Δ5′
 immunohistochemistry
 laboratory markers
 microsomal ethanol oxidizing system (MEOS)
 mithocondrion
K10plus-PPN:1700740377
Verknüpfungen:→ Zeitschrift

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