Journal
JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B
Volume 23, Issue 4, Pages 265-285Publisher
ZHEJIANG UNIV PRESS
DOI: 10.1631/jzus.B2100977
Keywords
Acetaminophen; Acetaminophen-induced liver injury; Hepatocyte necrosis; Sterile inflammation; Hepatocyte regeneration
Categories
Funding
- National Science and Technology Major Project of China [2018ZX10302206, 2017ZX10202203]
Ask authors/readers for more resources
This review summarizes three main mechanisms involved in the pathogenesis of acetaminophen-induced liver injury (AILI): hepatocyte necrosis, sterile inflammation, and hepatocyte regeneration. Relevant factors are discussed, and potential treatment options for AILI patients and promising novel strategies are described.
Acetaminophen, also known as N-acetyl-p-aminophenol (APAP), is commonly used as an antipyretic and analgesic agent. APAP overdose can induce hepatic toxicity, known as acetaminophen-induced liver injury (AILI). However, therapeutic doses of APAP can also induce AILI in patients with excessive alcohol intake or who are fasting. Hence, there is a need to understand the potential pathological mechanisms underlying AILI. In this review, we summarize three main mechanisms involved in the pathogenesis of AILI: hepatocyte necrosis, sterile inflammation, and hepatocyte regeneration. The relevant factors are elucidated and discussed. For instance, N-acetyl-p-benzoquinone imine (NAPQI) protein adducts trigger mitochondrial oxidative/nitrosative stress during hepatocyte necrosis, danger-associated molecular patterns (DAMPs) are released to elicit sterile inflammation, and certain growth factors contribute to liver regeneration. Finally, we describe the current potential treatment options for AILI patients and promising novel strategies available to researchers and pharmacists. This review provides a clearer understanding of AILI-related mechanisms to guide drug screening and selection for the clinical treatment of AILI patients in the future.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available