ArticleScientific reports2025
The hemopexin domain of matrix metalloproteinase-9 attenuates lipopolysaccharide-induced interleukin-6 secretion in liver.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Integrating Single-Cell Profiling with Generative AI forMolecules (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Matrix metalloproteinase-9 (MMP-9) has been implicated in modulating hepatic inflammation, as MMP-9 deficiency exacerbates liver damage and inflammatory responses in sepsis models. However, the mechanisms underlying its anti-inflammatory properties, particularly in the context of lipopolysaccharide (LPS) induced liver inflammation, remain poorly understood. Plasma and liver cytokine levels in MMP-9 catalytic-deficient mice were measured after the administration of 4.5 mg/kg LPS injections for 4 and 24 h. LPS-induced inflammatory responses were examined in mouse primary hepatocytes, hepatic, and macrophage cell lines by analyzing the secretion and expression of interleukin-6 (IL-6) in the gain- and loss-of-function of MMP-9. In vitro models were established by lentiviral infection, including MMP-9 knockout, Tet-On inducible wild-type MMP-9, and MMP-9 with catalytic domain mutation or hemopexin (PEX) domain deletion in wild-type parent cells. Following LPS treatment, MMP-9 catalytic-deficient mice demonstrated a significant increase in IL-6 levels, along with a notable decrease in MMP-9 protein expression relative to wild-type mice, in both plasma and liver tissue. Overexpression of MMP-9 significantly attenuated LPS-induced IL-6 secretion in hepatocytes. Notably, even the overexpression of a catalytically inactive MMP-9 mutant retained this suppressive effect. In contrast, deletion of the PEX domain abolished the inhibitory effect of MMP-9 on IL-6 secretion, indicating that the PEX domain, rather than its catalytic activity, is essential for this regulatory function. Moreover, MMP-9 overexpression markedly suppressed IL-6 secretion in response to LPS stimulation, whereas its genetic deletion significantly enhanced IL-6 secretion in macrophages. This study demonstrated that MMP-9 could partially protect the liver from LPS-induced damage by decreasing pro-inflammatory cytokine levels via its PEX domain, indicating the anti-inflammatory potential of the MMP-9 PEX domain against endotoxin.
Indexed as
Identifiers
What OpenQuestion holds
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.