NLRP3: a new therapeutic target in alcoholic liver disease.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 01 05 2023
accepted: 28 06 2023
medline: 23 10 2023
pubmed: 31 7 2023
entrez: 31 7 2023
Statut: epublish

Résumé

The liver is in charge of a wide range of critical physiological processes and it plays an important role in activating the innate immune system which elicits the inflammatory events. Chronic ethanol exposure disrupts hepatic inflammatory mechanism and leads to the release of proinflammatory mediators such as chemokines, cytokines and activation of inflammasomes. The mechanism of liver fibrosis/cirrhosis involve activation of NLRP3 inflammasome, leading to the destruction of hepatocytes and subsequent metabolic dysregulation in humans. In addition, increasing evidence suggests that alcohol intake significantly modifies liver epigenetics, promoting the development of alcoholic liver disease (ALD). Epigenetic changes including histone modification, microRNA-induced genetic modulation, and DNA methylation are crucial in alcohol-evoked cell signaling that affects gene expression in the hepatic system. Though we are at the beginning stage without having the entire print of epigenetic signature, it is time to focus more on NLRP3 inflammasome and epigenetic modifications. Here we review the novel aspect of ALD pathology linking to inflammation and highlighting the role of epigenetic modification associated with NLRP3 inflammasome and how it could be a therapeutic target in ALD.

Identifiants

pubmed: 37520548
doi: 10.3389/fimmu.2023.1215333
pmc: PMC10374212
doi:

Substances chimiques

Inflammasomes 0
NLR Family, Pyrin Domain-Containing 3 Protein 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1215333

Subventions

Organisme : CSRD VA
ID : I01 CX002084
Pays : United States
Organisme : NIAAA NIH HHS
ID : P50 AA030407
Pays : United States

Informations de copyright

Copyright © 2023 Brahadeeswaran, Dasgupta, Manickam, Saraswathi and Tamizhselvi.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Subhashini Brahadeeswaran (S)

Department of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.

Tiasha Dasgupta (T)

Department of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.

Venkatraman Manickam (V)

Department of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.

Viswanathan Saraswathi (V)

Department of Internal Medicine, Division of Diabetes, Endocrinology, and Metabolism, Veterans Affairs Medical Center, University of Nebraska Medical Center, Omaha, NE, United States.

Ramasamy Tamizhselvi (R)

Department of Biosciences, School of Biosciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.

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