Hepatic recruitment of the inflammatory Gr1+ monocyte subset upon liver injury promotes hepatic fibrosis

By K. Karlmark, Ralf Weiskirchen, H. Zimmermann, N. Gassler, Florent Ginhoux, Christian Weber, Miriam Merad, T. Luedde, Christian Trautwein, F. Tacke. Hepatology, 2009

797 citations recorded by the source corpus.

Subfields: Hepatology, Immunology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/00c8254bb282fe6a89548b1b39d90830c01df632

How researchers see this paper

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

In Hepatology

1. Natascha Roehlen
2. E. Crouchet
3. T. Baumert
4. F. Tacke
5. TA Wynn
6. Luke Barron
7. L. Hammerich

In Immunology

1. F. Tacke
2. Natascha Roehlen
3. E. Crouchet
4. T. Baumert
5. Luke Barron
6. TA Wynn
7. G. Randolph

In Pharmacology

1. TA Wynn

Citations in the corpus

• Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “Subsequent studies, however, revealed that a variety of cell types produce TGF-b1 following liver injury, including hepatocytes, sinusoidal endothelial cells, HSCs, Kupffer cells, CD4þ T cells, bone marrow–derived monocytes, and monocyte-derived macrophages, with the type of cellular injury likely i”
• Macrophages and Tissue Injury: Agents of Defense or Destruction? (2011, background): “Evidence for a role of this M2-derived growth factor in the fibrogenic process comes from findings that the development of fibrosis is prevented in CCR2 knockout mice and in mice treated with the Kupffer cell inhibitor methyl palmitate, and that this is directly correlated with decreased TGFβ produc”
• Origin and Functions of Tissue Macrophages (2014, background): “…of circulating monocytes (such as in CCR2- or MCP-1-deficient mice), fibrosis after acute liver injury or diet-induced nonalcoholic liver disease is reduced, suggesting that monocyte-derived macrophages rather than Kupffer cells promote liver fibrosis (Kassel et al., 2010; Karlmark et al., 2009).”
• Macrophage heterogeneity in liver injury and fibrosis. (2014, background): “The accumulation of these cells is likely based on two mechanisms: facilitated recruitment across inflamed sinusoidal endothelium and local transdifferentiation from CD14CD16 precursor cells [38], reminiscent of the maturation of murine Ly-6C to Ly-6C macrophages in experimental rodent liver injury ”
• Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Monocytes infiltration into the liver is primarily controlled by C-C Motif Chemokine Receptor 2 (CCR2) and its ligand CCL2 and is a major contributor of fibrosis development [82,83].”