ArticleWorld journal of gastroenterology2023
Effect and mechanism of reactive oxygen species-mediated NOD-like receptor family pyrin domain-containing 3 inflammasome activation in hepatic alveolar echinococcosis.
Article in World journal of gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- When Infection Meets Inflammation:Biology · 2026Review
- Quercetin prevents age-related hearing loss in C57BL/6J mice by activating mitophagy and inhibiting the NLRP3 inflammasome.PloS one · 2026Article
- The evaluation of inflammatory and immune composite markers for complications after deceased donor liver transplantation - a retrospective cohort study.Annals of medicine · 2025Article
- The key players of inflammasomes and pyroptosis in sepsis-induced pathogenesis and organ dysfunction.Frontiers in pharmacology · 2025Review
- The interactions between autophagy and immune in the liver-adipose-ovary circuit of polycystic ovary syndrome.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a significant component of the innate immune system that plays a vital role in the development of various parasitic diseases. However, its role in hepatic alveolar echinococcosis (HAE) remains unclear.
aimTo investigate the NLRP3 inflammasome and its mechanism of activation in HAE.
methodsWe assessed the expression of NLRP3, caspase-1, interleukin (IL)-1β, and IL-18 in the marginal zone and corresponding normal liver of 60 patients with HAE. A rat model of HAE was employed to investigate the role of the NLRP3 inflammasome in the marginal zone of HAE. Transwell experiments were conducted to investigate the effect of
resultsNLRP3 inflammasome activation was significantly associated with ROS. Inhibition of ROS production decreased NLRP3-caspase-1-IL-1β pathway activation and mitigated hepatocyte damage and inflammation.
conclusion
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Registered trials
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