ReviewCurrent rheumatology reports2015
Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis.
Review in Current rheumatology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 58 citations in OpenAlex.
- Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea.Dermatology practical & conceptual · 2024Article
- Review
- Novel role of long non-coding RNAs in autoimmune cutaneous disease.Journal of cell communication and signaling · 2022Review
- Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022Review
- Systemic Sclerosis: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2022Review
- Article
- Role of TLR4 Receptor Complex in the Regulation of the Innate Immune Response by Fibronectin.Cells · 2020Article
- Targeting the TLR signalosome with TIR domain-derived cell-permeable decoy peptides: the current state and perspectives.Innate immunity · 2020Review
- Exosomes in Systemic Sclerosis: Messengers Between Immune, Vascular and Fibrotic Components?International journal of molecular sciences · 2019Review
- Molecular biomarkers of Graves' ophthalmopathy.Experimental and molecular pathology · 2019Review
- Deciphering the Potential Pharmaceutical Mechanism of GUI-ZHI-FU-LING-WAN on Systemic Sclerosis based on Systems Biology Approaches.Scientific reports · 2019Article
- Inhibitive effect of TAK-242 on Tenon's capsule fibroblasts proliferation in rat eyes.International journal of ophthalmology · 2019Article
- Cross-Disease Innate Gene Signature: Emerging Diversity and Abundance in RA Comparing to SLE and SSc.Journal of immunology research · 2019Article
- Systemic Sclerosis Pathogenesis and Emerging Therapies, beyond the Fibroblast.BioMed research international · 2019Review
- The Long Non-coding RNA NRIR Drives IFN-Response in Monocytes: Implication for Systemic Sclerosis.Frontiers in immunology · 2019Article
- Immune complexes containing scleroderma-specific autoantibodies induce a profibrotic and proinflammatory phenotype in skin fibroblasts.Arthritis research & therapy · 2018Article
- Blocking TIR Domain Interactions in TLR9 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Novel insights into the role of inflammasomes in autoimmune and metabolic rheumatic diseases.Rheumatology international · 2018Review
- TLR4-dependent fibroblast activation drives persistent organ fibrosis in skin and lung.JCI insight · 2018Article
- Toll-like receptor 9 in systemic sclerosis patients: relation to modified Rodnan skin score, disease severity, and functional status.Clinical rheumatology · 2018Article
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
No grant is acknowledged in the PubMed record.
Abstract
Pathological fibrosis is a distinguishing hallmark of systemic sclerosis (SSc) as well as a number of more common conditions. Fibrosis is a complex and dynamic process associated with immune dysregulation, vasculopathy, and uncontrolled extracellular matrix production leading to intractable scar formation in the skin and internal organs. Persistent or recurrent chemical, infectious, mechanical, or autoimmune injury in genetically predisposed individuals causes sustained fibroblasts activation. Innate immune signaling via toll-like receptors (TLRs) is increasingly recognized as a key player driving the persistent fibrotic response in SSc. In particular, expression of TLR4 as well as its endogenous ligands are elevated in lesional tissue from patients with SSc. Ligand-induced TLR4 activation elicits potent stimulatory effects on fibrotic gene expression and myofibroblast differentiation. Furthermore, TLR4 appears to sensitize fibroblasts to the profibrotic stimulatory effect of transforming growth factor-β. This review highlights recent advances and emerging paradigms for understanding the regulation, complex functional roles, and therapeutic potential of TLRs in SSc pathogenesis.
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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.