Cell-to-Cell Communications in Alcohol-Associated Liver Disease.

Autor:	Osna NA; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States., Eguchi A; Department of Gastroenterology and Hepatology, Graduate School of Medicine, Mie University, Tsu, Japan., Feldstein AE; Department of Pediatrics, University of California, San Diego, San Diego, CA, United States., Tsukamoto H; Southern California Research Center for ALPD and Cirrhosis and Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, CA, United States.; Greater Los Angeles VA HealthCare System, Los Angeles, CA, United States., Dagur RS; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States., Ganesan M; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States., New-Aaron M; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Environmental Health, Occupational Health, and Toxicology, College of Public Health, University of Nebraska Medical Center, Omaha, NE, United States., Arumugam MK; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States., Chava S; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States., Ribeiro M; Harvard Medical School and Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States., Szabo G; Harvard Medical School and Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States., Mueller S; Salem Medical Center and Center for Alcohol Research, University of Heidelberg, Heidelberg, Germany., Wang S; Salem Medical Center and Center for Alcohol Research, University of Heidelberg, Heidelberg, Germany., Chen C; Salem Medical Center and Center for Alcohol Research, University of Heidelberg, Heidelberg, Germany., Weinman SA; Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS, United States., Kharbanda KK; Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE, United States.; Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, United States.; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in physiology [Front Physiol] 2022 Feb 21; Vol. 13, pp. 831004. Date of Electronic Publication: 2022 Feb 21 (Print Publication: 2022).
DOI:	10.3389/fphys.2022.831004
Abstrakt:	This review covers some important new aspects of the alcohol-induced communications between liver parenchymal and non-parenchymal cells leading to liver injury development. The information exchange between various cell types may promote end-stage liver disease progression and involves multiple mechanisms, such as direct cell-to-cell interactions, extracellular vesicles (EVs) or chemokines, cytokines, and growth factors contained in extracellular fluids/cell culture supernatants. Here, we highlighted the role of EVs derived from alcohol-exposed hepatocytes (HCs) in activation of non-parenchymal cells, liver macrophages (LM), and hepatic stellate cells (HSC). The review also concentrates on EV-mediated crosstalk between liver parenchymal and non-parenchymal cells in the settings of HIV- and alcohol co-exposure. In addition, we overviewed the literature on the crosstalk between cell death pathways and inflammasome activation in alcohol-activated HCs and macrophages. Furthermore, we covered highly clinically relevant studies on the role of non-inflammatory factors, sinusoidal pressure (SP), and hepatic arterialization in alcohol-induced hepatic fibrogenesis. We strongly believe that the review will disclose major mechanisms of cell-to-cell communications pertained to alcohol-induced liver injury progression and will identify therapeutically important targets, which can be used for alcohol-associated liver disease (ALD) prevention. Competing Interests: GS reports being a paid consultant for Evive Bio, Merck, Novartis, Durect Corporation, Terra Firma, Cyto Therapeutics, Pfizer, Surrozen; she holds stock in Glympse, Zomagen Biosciene/Ventyx Biosciences and receives royalties from Springer Nature Group and UpToDate Inc. All other authors reported no conflict of interests. (Copyright © 2022 Osna, Eguchi, Feldstein, Tsukamoto, Dagur, Ganesan, New-Aaron, Arumugam, Chava, Ribeiro, Szabo, Mueller, Wang, Chen, Weinman and Kharbanda.)
Databáze:	MEDLINE
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