Literature DB >> 35700755

Targeting innate immune responses to attenuate acetaminophen-induced hepatotoxicity.

Jincheng Wang1, Lulu Zhang1, Qi Shi2, Bo Yang1, Qiaojun He3, Jiajia Wang4, Qinjie Weng5.   

Abstract

Acetaminophen (APAP) hepatotoxicity is an important cause of acute liver failure, resulting in massive deaths in many developed countries. Currently, the metabolic process of APAP in the body has been well studied. However, the underlying mechanism of APAP-induced liver injury remains elusive. Increasing clinical and experimental evidences indicate that the innate immune responses are involved in the pathogenesis of APAP-induced acute liver injury (AILI), in which immune cells have dual roles of inducing inflammation to exacerbate hepatotoxicity and removing dead cells and debris to help liver regeneration. In this review, we summarize the latest findings of innate immune cells involved in AILI, particularly emphasizing the activation of innate immune cells and their different roles during the injury and repair phases. Moreover, current available treatments are discussed according to the different roles of innate immune cells in the development of AILI. This review aims to update the knowledge about innate immune responses in the pathogenesis of AILI, and provide potential therapeutic interventions for AILI.
Copyright © 2022 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Acetaminophen; Acute liver injury; Inflammation; Innate immune responses; Therapy

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Year:  2022        PMID: 35700755     DOI: 10.1016/j.bcp.2022.115142

Source DB:  PubMed          Journal:  Biochem Pharmacol        ISSN: 0006-2952            Impact factor:   6.100


  1 in total

1.  Antioxidant and chemoprotective peptides from simulated gastrointestinal digested (SGID) protein hydrolysate of Pyropia yezoensis against acetaminophen-induced HepG2 cells.

Authors:  Selvakumari Ulagesan; Taekil Eom; Taek-Jeong Nam; Youn-Hee Choi
Journal:  Bioprocess Biosyst Eng       Date:  2022-08-17       Impact factor: 3.434

  1 in total

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