ArticleWorld journal of gastroenterology2022
Fibrinogen-like protein 2 deficiency inhibits virus-induced fulminant hepatitis through abrogating inflammatory macrophage activation.
Article in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Hepatitis B Virus Variants and Cytokine Patterns in Acute Liver Failure and Transplant-Free Survival.Liver international : official journal of the International Association for the Study of the Liver · 2025Observational
- FPR1 signaling aberrantly regulates S100A8/A9 production by CD14Communications biology · 2024Article
- FGL1 and FGL2: emerging regulators of liver health and disease.Biomarker research · 2024Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHeterogeneous macrophages play an important role in multiple liver diseases, including viral fulminant hepatitis (VFH). Fibrinogen-like protein 2 (FGL2) is expressed on macrophages and regulates VFH pathogenesis; however, the underlying mechanism remains unclear.
aimTo explore how FGL2 regulates macrophage function and subsequent liver injury during VFH.
methodsMurine hepatitis virus strain 3 (MHV-3) was used to induce VFH in FGL2-deficient (
resultsFollowing MHV-3 infection, hepatic macrophages were largely replenished by proinflammatory monocyte-derived macrophages (MoMFs), which expressed high levels of FGL2. In
conclusionInfiltrated MoMFs represent a major source of hepatic inflammation during VFH progression, and FGL2 expression on MoMFs maintains the proinflammatory phenotype
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