ArticleScientific reports2020
Extracellular gp96 is a crucial mediator for driving immune hyperactivation and liver damage.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Expression of circulating GRP78 and gp96, endoplasmic reticulum stress-related proteins, in menstrual and bladder pain sensitivity.Scientific reports · 2026Article
- Heat shock protein Gp96 (Grp94) in malaria: functional insights at the host-parasite interface and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- The Role and Phagocytic Mechanisms of Alveolar Macrophages in Inflammatory Responses Induced by Diesel Exhaust Particles.Environmental science & technology · 2025Article
- Manipulation of Surface Potential Distribution Enhances Osteogenesis by Promoting Pro-Angiogenic Macrophage Polarization via Activation of the PI3K-Akt Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cell- and Serum-Derived Proteins Act as DAMPs to Activate RAW 264.7 Macrophage-like Cells on Silicone Implants.ACS biomaterials science & engineering · 2024Article
- Associations of Wnt5a expression with liver injury in chronic hepatitis B virus infection.BMC infectious diseases · 2023Article
- Cirrhosis-associated immune dysfunction.Nature reviews. Gastroenterology & hepatology · 2022Review
- Plasma gp96 is a Novel Predictive Biomarker for Severe COVID-19.Microbiology spectrum · 2021Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Liver failure leads to the massive necrosis of hepatocytes, releasing large amounts of intracellular components including damage-associated molecular patterns (DAMPs). We found that extracellular gp96 levels in serum were elevated in patients with chronic hepatitis B infection (CHB) and acute-on-chronic liver failure (ACLF). Meanwhile, the gp96 level positively correlated with hepatic necroinflammation. We employed two mouse liver damage and liver failure models induced by lipopolysaccharide (LPS) plus D-galactosamine (D-Galn), and concanavalin A (ConA) to identify the function of extracellular gp96. As a result, the inhibition of extracellular gp96 by a specific peptide efficiently mitigated both LPS/D-Galn- and ConA-induced liver injury and immune hyperactivation, whereas exogenous gp96 aggravated the symptoms of hepatic injury in mice but not in Kupffer cells-ablated mice. The exposure of Kupffer cells to gp96 induced the secretion of pro-inflammatory cytokines. Collectively, our data demonstrate that gp96 released from necrotic hepatocytes aggravates immune hyperactivation and promotes liver damage and possibly the development of liver failure mainly by activating Kupffer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.