Evidence map›Paper›PMID 42909202›Full record

ArticleFrontiers in pharmacology2026

P2X7 receptor contributes to hepatic inflammation and collagen deposition in methionine- and choline-deficient diet-fed mice.

Sthefani Rodrigues Batista da Silva, Fabiana Cristina-Rodrigues, Mariana M Chaves, Isabele Pinheiro Cruz, Lorraine de Oliveira da Cruz, Maria Fernanda Carvalho de Araujo, Soraia das Neves Vieira Cavalcanti, Georgia Correa Atella, Christina Maeda Takiya, Luiz Eduardo Baggio Savio and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Sthefani Rodrigues Batista da Silva *Laboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Fabiana Cristina-Rodrigues *Laboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Mariana M Chaves *Laboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Isabele Pinheiro CruzLaboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Lorraine de Oliveira da CruzLaboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Maria Fernanda Carvalho de AraujoLaboratory of Biochemistry of Lipids and Lipoproteins, Leopoldo de Meis Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Soraia das Neves Vieira CavalcantiLaboratory of Biochemistry of Lipids and Lipoproteins, Leopoldo de Meis Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Georgia Correa AtellaLaboratory of Biochemistry of Lipids and Lipoproteins, Leopoldo de Meis Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Christina Maeda TakiyaLaboratory of Immunopathology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Luiz Eduardo Baggio SavioLaboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Robson Coutinho-SilvaLaboratory of Immunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Metabolic-Dysfunction-Associated Steatohepatitis (MASH) is characterized by hepatic steatosis, inflammation, and progressive liver injury, with growing evidence implicating purinergic signaling and inflammasome activation in disease progression. Here, we investigated the role of the P2X7 receptor and caspase-1/11 signaling in methionine- and choline-deficient (MCD) diet-induced liver injury in mice. Methods: Mice were fed an MCD diet to induce liver injury, and hepatic steatosis, inflammation, and tissue injury were assessed by histopathological analysis. Hepatic triacylglycerol and cholesterol accumulation, Results: MCD diet feeding induced significant weight loss and marked histopathological alterations, including hepatic steatosis, inflammatory infiltrates, and hepatocellular injury, accompanied by increased hepatic triacylglycerol and cholesterol accumulation. Hepatic injury was partially dependent on caspase-1/11 signaling, whereas hepatic inflammation was partially dependent on the P2X7 receptor. Although Discussion: Together, these findings demonstrate that the P2X7 receptor and caspase-1/11 play a role in amplifying inflammatory responses and reshaping the hepatic purinergic microenvironment during steatohepatitis progression, highlighting the P2X7 receptor as a potential therapeutic target in chronic liver disease.

Indexed as

chronic liver diseaseinflammasomemetabolic dysfunction-associated steatohepatitismethionine- and choline-deficient dietP2X7 receptor

Identifiers

PMID42909202
PMCPMC13683839

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.