The DOI matches its Crossref record; 79 of the 80 references it cites were found in a registry or an index.
Resolution of inflammation: the beginning programs the end
Abstract
Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid-derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence. Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-beta1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics. Understanding these and further details of the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In conclusion, attenuating inflammation itself might also interfere with successful resolution, since the process of resolution is initiated already very early during the inflammatory process.441”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [441]
In the citing paper
“Conceptually, results of our study support the idea that excessive fibrotic response is a direct result of a “failed” resolution of sterile inflammation35, with impaired phagocytosis of injured hepatocytes enabling exposure of quiescent stellate cells to fibrogenic mito-DAMPs.”
From Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis (2020) · cites this paper as [35]
In the citing paper
“Thus, PPAR␥ is important to shape an anti-inflammatory macrophage phenotype and appears crucial for dampening inflammation (15).”
From MicroRNA-27b Contributes to Lipopolysaccharide-mediated Peroxisome Proliferator-activated Receptor γ (PPARγ) mRNA Destabilization (2010) · cites this paper as [15]
Citations
Cites
Prostaglandins and Leukotrienes: Advances in Eicosanoid Biology
Funk, C. D. (2001) · Science · doi:10.1126/science.294.5548.1871 · Cited by 3,817
Fadok, V. A., Bratton, D. L., Konowal, A., Freed, P. W., Westcott, J. Y., & Henson, P. M. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1112 · Cited by 3,166
Points of control in inflammation
Nathan, C. (2002) · Nature · doi:10.1038/nature01320 · Cited by 2,738
Inflammation. Basic principles and clinical correlates
(1989) · Biomedicine & Pharmacotherapy · doi:10.1016/0753-3322(89)90156-x · Cited by 2,388
Leukotrienes and Lipoxins: Structures, Biosynthesis, and Biological Effects
Samuelsson, B. O., Dahlén, S., LINDGREN, J. Å., Rouzer, C. A., & Serhan, C. N. (1987) · Science · doi:10.1126/science.2820055 · Cited by 2,233
Self-citationImmunosuppressive effects of apoptotic cells
Voll, R. E., Herrmann, M., Roth, E. A., Stach, C., Kalden, J. R., & Girkontaite, I. (1997) · Nature · doi:10.1038/37022 · Cited by 1,787
Serhan, C. N., Hong, S., Gronert, K., Colgan, S. P., Devchand, P. R., Mirick, G., & Moussignac, R.-L. (2002) · The Journal of Experimental Medicine · doi:10.1084/jem.20020760 · Cited by 1,650
Self-citationA blast from the past: clearance of apoptotic cells regulates immune responses
Savill, J., Dransfield, I., Gregory, C. D., & Haslett, C. (2002) · Nature reviews. Immunology · doi:10.1038/nri957 · Cited by 1,574
Self-citationSavill, J. S., Wyllie, A. H., Henson, J. E., Walport, M. J., Henson, P. M., & Haslett, C. (1989) · Journal of Clinical Investigation · doi:10.1172/jci113970 · Cited by 1,536
Self-citation
Research works printed but not linked: 1
- Hurley, J.V. in Acute inflammation (ed. Hurley, J.V.) 109–117 (Churchill Livingstone, London, 1983).
Cited by
Sorted by citations
Items 1,001–1,005 of 1,005
Everts, P. A., Mazzola, T., Mautner, K., Randelli, P. S., & Podesta, L. (2022) · Biomedicines · doi:10.3390/biomedicines10112933 · Cited by 34
Souza, C. M. M., de Lima, D. C., Bastos, T. S., de Oliveira, S. G., Beirão, B. C. B., & Félix, A. P. (2019) · Animal Science Journal · doi:10.1111/asj.13294 · Cited by 31
Nasopoulou, C., Karantonis, H. C., Detopoulou, M., Demopoulos, C. A., & Zabetakis, I. (2014) · Phytochemistry Reviews · doi:10.1007/s11101-014-9350-8 · Cited by 26
Morin, C., Charbonneau, L., Ouellet, N., Ouellet, H., Blier, P. U., Dufresne, F., & Fortin, S. (2017) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2017.05.018 · Cited by 16
Exploring the Prognosis-Related Genetic Variation in Gastric Cancer Based on mGWAS
Zhang, Y., Lyu, Y., Chen, L., Cao, K., Chen, J., He, C., Lyu, X., Jiang, Y., Xiang, J., Liu, B., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242015259 · Cited by 5
Metadata
- Authors
- Serhan, C. N., & Savill, J.
- Affiliations
- Brigham and Women's Hospital (US)
- Centre for Inflammation Research (GB)
- Corresponding author
- Serhan, Charles N
- Venue
- Nature Immunology
- Published
- 2005-11-17
- Volume
- 6
- Issue
- 12
- Pages
- 1191-1197
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2004536682
- Cited by
- 2,552
- References
- 80
- Citations by year
- 2026: 107 · 2025: 94 · 2024: 105 · 2023: 119 · 2022: 141 · 2021: 153 · 2020: 131 · 2019: 123 · 2018: 117 · 2017: 137 · 2016: 100 · 2015: 128 · 2014: 161 · 2013: 157 · 2012: 139
- FWCI
- 11.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- National Institute of General Medical Sciences (GM 38765)
- National Institute of Dental and Craniofacial Research (P50DE016191)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
- Keywords
- inflammation resolution, acute inflammation, lipoxins, resolvins, protectins, omega-3 polyunsaturated fatty acids, arachidonic acid metabolites, prostaglandins, leukotrienes, neutrophil apoptosis, neutrophil clearance, macrophage phagocytosis, TGF-β1, anti-inflammatory cytokines, anti-inflammatory drug development
- MeSH terms
- Acute Disease, Animals, Humans, Inflammation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review