ReviewToxicologic pathology2012
Cellular regulation of the inflammatory response.
Review in Toxicologic pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- Research on the signaling pathway and the related mechanism of traditional Chinese medicine intervention in chronic gastritis of the "inflammation-cancer transformation".Frontiers in pharmacology · 2024Review
- Anti-Inflammatory Properties of Plants from Serbian Traditional Medicine.Life (Basel, Switzerland) · 2023Review
- Inflammatory Effects ofToxins · 2021Review
- Lactobacillus rhamnosus Affects Rat Peritoneal Cavity Cell Response to Stimulation with Gut Microbiota: Focus on the Host Innate Immunity.Inflammation · 2021Article
- Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation.Journal of neuroinflammation · 2021Review
- Anti-Inflammatory Effect of Musa acuminata Stem.European journal of dentistry · 2020Article
- Stem Cell Extracellular Vesicles: Extended Messages of Regeneration.Annual review of pharmacology and toxicology · 2017Review
- The Neutrophil Response Induced by an Agonist for Free Fatty Acid Receptor 2 (GPR43) Is Primed by Tumor Necrosis Factor Alpha and by Receptor Uncoupling from the Cytoskeleton but Attenuated by Tissue Recruitment.Molecular and cellular biology · 2016Article
- Anti-Inflammatory Effects of 6,8-Diprenyl-7,4'-dihydroxyflavanone from Sophora tonkinensis on Lipopolysaccharide-Stimulated RAW 264.7 Cells.Molecules (Basel, Switzerland) · 2016Article
- Apoptotic cells trigger a membrane-initiated pathway to increase ABCA1.The Journal of clinical investigation · 2015Article
- Article
- Endogenous and exogenous cell-based pathways for recovery from acute respiratory distress syndrome.Clinics in chest medicine · 2014Review
- Role of biphasic changes in splenic dendritic cell activity in a mouse model of multiple organ dysfunction syndrome.International journal of clinical and experimental pathology · 2014Article
- Redox control of inflammation in macrophages.Antioxidants & redox signaling · 2013Review
- Curcumin alleviates immune-complex-mediated glomerulonephritis in factor-H-deficient mice.Immunology · 2013Article
- Impact of microbes on autoimmune diseases.Archivum immunologiae et therapiae experimentalis · 2013Review
- Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague.PLoS pathogens · 2013Article
- Propofol reduces lipopolysaccharide-induced, NADPH oxidase (NOX 2) mediated TNF- α and IL-6 production in macrophages.Clinical & developmental immunology · 2013Article
- Inflammatory biomarkers in workers exposed to silica dust: integrative review.Revista brasileira de medicina do trabalho : publicacao oficial da Associacao Nacional de Medicina do Trabalho-ANAMTReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In simple terms, inflammation can be defined as a beneficial, nonspecific response of tissues to injury that generally leads to restoration of normal structure and function. In this concept, resolution of the inflammatory response, once it has achieved its protective and pro-immunogenic functions, becomes a critical determinant of what might be considered the paradox of inflammation. On one hand, inflammation is essential to resolve tissue injury and maintain homeostasis. On the other, inflammation is a key participant in the great majority of human diseases. Accordingly, to achieve complete resolution of inflammation, it is necessary to both turn off inflammatory mediator production and inflammatory cell accumulation and to remove inflammatory cells and debris without initiating an autoimmune response. Much of this process involves key activities of the mononuclear phagocyte series of cells, including resident and recruited macrophages. Recognition of activated and dying acute inflammatory cells by mononuclear phagocytes has been shown to (a) enhance macropinocytic activity for removal of debris, (b) enhance uptake of the effete inflammatory cells themselves, (c) induce inflammosuppressive and immunosuppressive mediators such as TGFβ and IL-10 that can down-regulate and limit proinflammatory mediator production, and (d) induce production of growth factors for tissue cells that may play key roles in tissue repair. Defects in these highly regulated processes are associated with persistent inflammation and/or autoimmunity in overaggressive resolution mechanisms such as nonresolving fibrosis or persistent tissue destruction as in emphysema.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.