Nonresolving inflammation.

By C. Nathan, A. Ding. Cell, 2010

1,752 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9995ae1cb56bb0043ed5c1774b39e1939b72366d

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. A. Mantovani
2. A. Lichtman
3. TA Wynn
4. Subhra K. Biswas
5. S. Gordon
6. J. Hamilton
7. A. Sica
8. P. Murray

In Immunology

1. A. Mantovani
2. A. Sica
3. S. Gordon
4. TA Wynn
5. F. Martínez
6. P. Murray
7. Subhra K. Biswas
8. M. Locati

In Molecular Biology

1. S. Gordon
2. A. Lichtman
3. C. Deutschman
4. A. Mantovani
5. A. Sica
6. Andrew H. Miller
7. Charles L Raison
8. Subhra K. Biswas

Citations in the corpus

• Macrophage Polarization States in the Tumor Microenvironment (2021, background): “Inflammation can lead to further inflammation through tissue damage and necrosis, making the resolution of inflammation even more critical and highlighting the importance of macrophages in this process [62].”
• The Multifaceted Role of Annexin A1 in Viral Infections (2023, background): “In chronic inflammation, there is a predominance of macrophages, fibroblasts and an intense formation of fibrotic tissue [28].”
• Zinc in Infection and Inflammation (2017, background): “However, sometimes the inflammation does not resolve and later becomes chronic, leading to loss of tissue function [38].”
• A genomic storm in critically injured humans (2011, background): “The findings are most consistent with the nonresolving inflammation hypothesis (Nathan and Ding, 2010) that severely injured patients who are destined to die from their injuries have the same response as patients who subsequently recover.”
• Monocyte-Macrophages and T Cells in Atherosclerosis (2017, positive): “Resolution of Inflammation Is Impaired in Atherosclerosis and Contributes to Plaque Progression In normal physiology, the inflammatory response is directly linked to a resolution phase that repairs collateral damage and restores tissue homeostasis (Serhan et al., 2007; Nathan and Ding, 2010).”
• Homeostasis, Inflammation, and Disease Susceptibility (2015, neutral): “The non-resolving inflammation may, in turn, account for the persistence of chronic diseases (Nathan and Ding, 2010; Serhan et al., 2007).”
• Sepsis: current dogma and new perspectives. (2014, background): “…of resolvins that accelerate the efflux of inflammatory cells and debris, and feedback from the nervous system that suppresses the release of inflammatory mediators and stimulates the release of resolvins (Nathan and Ding, 2010; Schwab et al., 2007; Medzhitov, 2010; Andersson and Tracey, 2012a).”
• Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “When activated out of sequence, however, macrophages have the potential to interrupt different phases of repair and persistent macrophage activation can lead to maladaptive, chronic inflammation and dysfunctional wound healing (Werdin et al., 2009; Nathan and Ding, 2010).”