ArticleThe open rheumatology journal2012
New insights into the mechanisms of innate immune receptor signalling in fibrosis.
Article in The open rheumatology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed.
- Novel role of long non-coding RNAs in autoimmune cutaneous disease.Journal of cell communication and signaling · 2022Review
- Prevention of bleomycin-induced pulmonary fibrosis by a RANKL peptide in mice.Scientific reports · 2022Article
- Uncommon presentation of morphea related to interferon beta in a patient with concomitant multiple sclerosis and chronic hepatitis C: A case report.Clinical case reports · 2020Article
- Biological approaches for hypertrophic scars.International wound journal · 2020Review
- C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells.Bioscience reports · 2019Article
- Circulating and inducible IL-32α in chronic hepatitis C virus infection.Canadian liver journal · 2019Article
- The Long Non-coding RNA NRIR Drives IFN-Response in Monocytes: Implication for Systemic Sclerosis.Frontiers in immunology · 2019Article
- Phycocyanin attenuates pulmonary fibrosis via the TLR2-MyD88-NF-κB signaling pathway.Scientific reports · 2017Article
- Obesity-associated extracellular mtDNA activates central TGFβ pathway to cause blood pressure increase.American journal of physiology. Endocrinology and metabolism · 2017Article
- Taking the STING out of TLR-driven autoimmune diseases: good, bad, or indifferent?Journal of leukocyte biology · 2017Review
- The Lung Microbiome, Immunity, and the Pathogenesis of Chronic Lung Disease.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- Update on macrophages and innate immunity in scleroderma.Current opinion in rheumatology · 2015Review
- MicroRNAs as potential targets for progressive pulmonary fibrosis.Frontiers in pharmacology · 2015Review
- Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis.Current rheumatology reports · 2015Review
- Cytokine profiles in the joint depend on pathology, but are different between synovial fluid, cartilage tissue and cultured chondrocytes.Arthritis research & therapy · 2014Article
- Identification of gene microarray expression profiles in patients with chronic graft-versus-host disease following allogeneic hematopoietic cell transplantation.Clinical immunology (Orlando, Fla.) · 2013Article
- Probiotics as a novel treatment for non-alcoholic Fatty liver disease; a systematic review on the current evidences.Hepatitis monthly · 2013Article
- Oxidative stress and pulmonary changes in experimental liver cirrhosis.Oxidative medicine and cellular longevity · 2012Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Recent advances in our understanding of innate immunity and inflammation have direct bearing on how we understand autoimmunity, and fibrosis, and how innate immune sensors might stimulate both of these key features of several fibrotic diseases. Toll-like receptors (TLRs) are the major receptors for recognizing pathogen associated molecular patterns present on bacterial cell walls, such as LPS, and nucleic acids (RNA and DNA). Several intracellular pathways mediate TLR effects and initiate various pro-inflammatory programs. Mechanisms for control of inflammation, matrix remodeling, and ultimately fibrosis are also activated. Transforming growth factor-beta (TGF-β), Interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-13 (IL-13), and interferon (IFNs) appear particularly important in regulating pro-fibrotic aspects of innate immune activation. These mechanisms appear important in fibrotic disease affecting multiple organ-systems, including lung, liver, kidney, and skin. These observations provide new paradigms for understanding the relationship between immunity/inflammation and fibrosis, however, the precise ligand and mechanism linking innate immune sensor(s) to fibrosis remain uncertain in most illnesses.
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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.