IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice.

By J. Petrášek, S. Bala, T. Csák, D. Lippai, K. Kodys, V. Menashy, Matthew Barrieau, S. Min, E. Kurt-Jones, G. Szabo. Journal of Clinical Investigation, 2012

678 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/042e3ded1c5f1c675bb0ac865ba0ff89f862da7d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Christopher D. Byrne
2. M. Pinzani
3. G. Targher
4. Herbert Tilg
5. E. Seki
6. Robert F. Schwabe
7. M. Parola
8. Ali Canbay

In Molecular Biology

1. Christopher D. Byrne
2. Kate Schroder
3. Robert F. Schwabe
4. S. Masters
5. Herbert Tilg
6. G. Targher

In Pathology and Forensic Medicine

1. Christopher D. Byrne
2. Herbert Tilg
3. M. Pinzani
4. M. Parola
5. G. Targher

Citations in the corpus

• Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways (2015, background): “Alcoholmediated hepatocyte injury, through generation of acetaldehyde and ROS, increases the production of ROS, TNF-a, IL-1b, TGF-b, and CCL2 in the liver, predominantly through macrophages.(54,98) In part, increased inflammation in ALD is mediated by increased translocation of intestinal bacterial ”
• NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice (2017, background): “Our data also fail to support a proposed role of IL-1 in contributing to hepatocyte fat deposition in NASH [17,49].”
• NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation and fibrosis (2014, background): “appears to be mediated through the NLRP3 inflammasome.(15-17) These studies demonstrate that Casp1 plays an important role in inflammation and fibrosis during NASH and ASH development.”
• Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues. (2019, background): “MFs acquire the ability to migrate in a scenario of progressive CLD in response to several peptide chemoattractants released by surrounding liver cell populations or by MFs themselves and/or trapped in the ECM, including PDGF, CCL2, Angiotensin II, VEGF-A and Angiopoietin 1.”
• MASLD: a systemic metabolic disorder with cardiovascular and malignant complications (2024, background): “40 41 Chronic liver inflammation is a major driver of liver fibrosis and further complications of MASLD, both inside and outside of the liver.”