Liver macrophages in tissue homeostasis and disease

By O. Krenkel, F. Tacke. Nature reviews. Immunology, 2017

1,263 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/a8cd6698234253a14b2242fb62533858a2583f6f

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. M. Parola
2. S. Friedman
3. M. Pinzani
4. Natascha Roehlen
5. E. Crouchet
6. T. Baumert
7. Gerald I. Shulman
8. R. Loomba

In Hepatology

1. M. Parola
2. S. Friedman
3. M. Pinzani
4. T. Baumert
5. Natascha Roehlen
6. E. Crouchet
7. Gerald I. Shulman
8. R. Loomba

In Immunology

1. Sandra Hervás-Stubbs
2. M. Pinzani
3. I. Melero
4. Gerald I. Shulman
5. Natascha Roehlen
6. M. Parola
7. S. Friedman
8. E. Crouchet

Citations in the corpus

• Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “While being difficult to distinctly attribute this dichotomous classification to pro- or anti-fibrogenic actions [13,15], numerous studies indicate distinct subpopulations of macrophages to coexist in the liver and to contribute to different phases of fibrosis.”
• Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues. (2019, background): “extremely complex scenario that is currently superseding the traditional and schematic distinction between M1 and M2 polarization (Krenkel and Tacke, 2017; Tacke, 2017).”
• Advances in immunotherapy for hepatocellular carcinoma (2021, background): “I.M. receives funding from MINECO SAF2014-52361-R and SAF 2017- 83267-C2-1R; Worldwide Cancer Research Grant (15-1146); the Asociacion Española Contra el Cancer (AECC) Foundation under grant GCB15152947MELE; and the European Union’s Horizon 2020 Program (grant agreement no. 635122 PROCROP).”
• Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Pathways driven by macrophages include not only inflammation and fibrosis but also steatosis through secretion of IL-1b, tumor necrosis factor alpha (TNF-a), the CCL2 chemokine, and MCP-1 (Krenkel and Tacke, 2017).”
• NAFLD and increased risk of cardiovascular disease: clinical associations, pathophysiological mechanisms and pharmacological implications (2020, neutral): “44 45 It has also to be acknowledged that inflammation might be present in the liver intermittently and/or in a chronic-relapsing manner.”