Mechanisms and biomarkers of liver regeneration after drug-induced liver injury.

Acetaminophen Acute liver failure Alcohol Carbon tetrachloride Cytokines Drug-induced liver injury Growth factors Hepatocyte proliferation Ischemic hepatitis Liver repair

Journal

Advances in pharmacology (San Diego, Calif.)
ISSN: 1557-8925
Titre abrégé: Adv Pharmacol
Pays: United States
ID NLM: 9015397

Informations de publication

Date de publication:
2019
Historique:
entrez: 17 7 2019
pubmed: 17 7 2019
medline: 13 2 2020
Statut: ppublish

Résumé

Liver, the major metabolic organ in the body, is known for its remarkable capacity to regenerate. Whereas partial hepatectomy (PHx) is a popular model for the study of liver regeneration, the liver also regenerates after acute injury, but less is known about the mechanisms that drive it. Recent studies have shown that liver regeneration is critical for survival in acute liver failure (ALF), which is usually due to drug-induced liver injury (DILI). It is sometimes assumed that the signaling pathways involved are similar to those that regulate regeneration after PHx, but there are likely to be critical differences. A better understanding of regeneration mechanisms after DILI and hepatotoxicity in general could lead to development of new therapies for ALF patients and new biomarkers to predict patient outcome. Here, we summarize what is known about the mechanisms of liver regeneration and repair after hepatotoxicity. We also review the literature in the emerging field of liver regeneration biomarkers.

Identifiants

pubmed: 31307589
pii: S1054-3589(19)30014-6
doi: 10.1016/bs.apha.2019.03.001
pmc: PMC7641498
mid: NIHMS1639530
pii:
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

241-262

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM103549
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM118247
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK098414
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM106999
Pays : United States

Informations de copyright

© 2019 Elsevier Inc. All rights reserved.

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Auteurs

Melissa M Clemens (MM)

Interdisciplinary Biomedical Sciences Graduate Program, University of Arkansas for Medical Sciences, Little Rock, AR, United States.

Mitchell R McGill (MR)

Department of Environmental and Occupational Health, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR, United States; Department of Pharmacology and Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, United States. Electronic address: mmcgill@uams.edu.

Udayan Apte (U)

Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, KS, United States.

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Classifications MeSH