ArticleFrontiers in immunology2026
GHSR and TLR4 collectively promote hepatic inflammation and aberrant repair in alveolar echinococcosis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Background and objective: Alveolar echinococcosis (AE) is a fatal zoonotic parasitic disease that causes progressive hepatic injury through chronic inflammation, aberrant proliferative repair, and liver fibrosis. GHSR and TLR4 individually regulate hepatic inflammation and proliferation; however, their synergistic roles in Methods: Wild-type (WT), GHSR-knockout (GHSR Results: Knockout of either GHSR or TLR4 alleviated AE-induced hepatic lesions, fibrosis, and liver dysfunction. Mechanistically, their deletion suppressed PI3K/Akt-mediated proliferation and TLR4/MyD88/NF-κB-mediated inflammation, reduced M1/M2 macrophage infiltration, decreased pro-inflammatory cytokines (IL-6, TNF-α, and TGF-β1), and elevated anti-inflammatory IL-10. A positive expression correlation between GHSR and TLR4 was confirmed in AE, Proteomics further verified their coordinated modulation of hepatic inflammation and aberrant repair. Conclusions: Collectively, upregulated GHSR and TLR4 jointly promote Echinococcus multilocularis-associated hepatic damage via sustaining persistent inflammation and dysregulated proliferative tissue repair. This study demonstrates coordinated pro-pathological involvement of GHSR and TLR4 in AE progression and provides
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