ReviewImmunology letters2018
Endogenous ligands of TLR4 promote unresolving tissue fibrosis: Implications for systemic sclerosis and its targeted therapy.
Review in Immunology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Calprotectin (S100A8/S100A9): a key protein between inflammation and cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Pooled it
- Identification and validation of lymphangiogenesis-related genes for predicting acute myeloid leukemia prognosis: insights from bulk RNA sequencing and single-cell RNA sequencing analyses.Clinical and experimental medicine · 2026Article
- Th17-related genes PGAP1 and TMBIM1 serve as potential diagnostic and predictive biomarkers in systemic sclerosis: bioinformatic identification and murine model validation.Clinical rheumatology · 2026Article
- Article
- A dermis-on-a-chip model for compound screening.Materials today. Bio · 2025Article
- The role of TLR-4 in chemoresistance of cancer.Discover oncology · 2025Review
- The Soluble Cytoplasmic Tail of CD45 (ct-CD45) Regulates Dendritic Cell Activation and Function via TLR4 Signaling.International journal of molecular sciences · 2025Article
- Cell autonomous TLR4 signaling modulates TGF-β induced activation of human cardiac fibroblasts.Heliyon · 2025Article
- MR molecular imaging for monitoring and predicting tumor responses to immunotherapy.Theranostics · 2025Article
- Inhibiting triggering receptor expressed on myeloid cells 1 signaling to ameliorate skin fibrosis.JCI insight · 2024Article
- Critical Analysis of Cytoplasmic Progression of Inflammatory Signaling Suggests Potential Pharmacologic Targets for Wound Healing and Fibrotic Disorders.Biomedicines · 2024Review
- Review
- Prevalence of hybrid TLR4Frontiers in immunology · 2024Article
- Extracellular Matrix-Derived Damage-Associated Molecular Patterns (DAMP): Implications in Systemic Sclerosis and Fibrosis.The Journal of investigative dermatology · 2023Review
- S100A8 and S100A9 are associated with endometrial shedding during menstruation.Medical molecular morphology · 2023Article
- Induction of pro-inflammatory genes by fibronectin DAMPs in three fibroblast cell lines: Role of TAK1 and MAP kinases.PloS one · 2023Article
- The Microbiome in Systemic Sclerosis: Pathophysiology and Therapeutic Potential.International journal of molecular sciences · 2022Review
- Deficiency of inhibitory TLR4 homolog RP105 exacerbates fibrosis.JCI insight · 2022Article
- Binding of Gamma-Glutamyl Transferase to TLR4 Signalling Allows Tissue Factor Activation in Monocytes.International journal of molecular sciences · 2022Article
- Innate Immunity Mechanisms in Marine Multicellular Organisms.Marine drugs · 2022Review
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
Fibrosis, the hallmark of scleroderma or systemic sclerosis (SSc), is a complex, dynamic and generally irreversible pathophysiological process that leads to tissue disruption, and lacks effective therapy. While early-stage fibrosis resembles normal wound healing, in SSc fibrosis fails to resolve. Innate immune signaling via toll-like receptors (TLRs) has recently emerged as a key driver of persistent fibrotic response in SSc. Recurrent injury in genetically predisposed individual causes generation of "damage-associated molecular patterns" (DAMPs) such as fibronectin-EDA and tenascin-C. Sensing of these danger signals by TLR4 on resident cells elicits potent stimulatory effects on fibrotic gene expression and myofibroblast differentiation, and appears to sensitize fibroblasts to the profibrotic stimulatory effect of TGF-β. Thus, DAMPs induce TLR4-mediated innate immune signaling on resident mesenchymal cells which drives the emergence and persistence of fibrotic cells in tissues, and underlies the switch from a self-limited repair response to non-resolving pathological fibrosis characteristic of SSc. In this review, we present current views of the DAMP-TLR4 axis in driving sustained fibroblasts activation and its pathogenic roles in fibrosis progression in SSc, and potential anti-fibrotic approaches for selective therapeutic targeting of TLR4 signaling.
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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.