ReviewBiomolecules2021
Organ Fibrosis and Autoimmunity: The Role of Inflammation in TGFβ-Dependent EMT.
Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Recent Update on the Anti-Inflammatory Activities of Propolis.Molecules (Basel, Switzerland) · 2022Pooled it
- Spatially resolved single cell atlas deciphers SAA1 inflammatory epithelial cells.International journal of oral science · 2026Article
- A human ex vivo model of radiation-induced skin injury recapitulates p53-driven profibrotic response to radiotherapy.JCI insight · 2026Article
- ECMSim: A high-performance interactive web application for real-time spatiotemporal simulation of cardiac ECM signaling and diffusion.Matrix biology plus · 2026Article
- β-Klotho inhibited the epithelial-mesenchymal transition of liver sinusoidal endothelial cells to alleviate schistosomiasis liver fibrosis.PLoS pathogens · 2026Article
- Curcumin suppresses EMT to alleviate oral submucous fibrosis progression through XIST/miR-25-3p-mediated inactivation of the TGF-β1/Smads signalling pathway.International dental journal · 2026Article
- The pathogenesis of müller cell glial-mesenchymal transition in retinal fibrosis-related eye diseases.Frontiers in cell and developmental biology · 2026Review
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- SHP1 overexpression ameliorates renal fibrosis via inhibition of STAT3 signaling and glycolysis reprogramming.Scientific reports · 2025Article
- Article
- Differences in Expression of Epithelial-Mesenchymal Transition (EMT) Induction Genes TGF-Β Pathway Transition in Colorectal Cancer Patients Non-Metastatic and Metastatic.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Computational Drug Repurposing Screening Targeting Profibrotic Cytokine in Acute Respiratory Distress Syndrome.Cell biochemistry and biophysics · 2025Article
- Review
- Article
- Mechanism of Astragalus Polysaccharide in Alleviating Bovine Mammary Fibrosis Through ROS/NLRP3 Inhibition and EMT Regulation.Antioxidants (Basel, Switzerland) · 2025Article
- TGF-β/SMAD Pathway Mediates Cadmium Poisoning-Induced Chicken Liver Fibrosis and Epithelial-Mesenchymal Transition.Biological trace element research · 2025Article
- AAV-IKV mediated expression of decorin inhibits EMT and fibrosis in a murine model of Glaucoma and AAV-IKV transduction in Non-Human Primates.Scientific reports · 2025Article
- Review
- Mechanisms of EMT in the immune microenvironment of plasma cell mastitis.Frontiers in immunology · 2025Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent advances in our understanding of the molecular pathways that control the link of inflammation with organ fibrosis and autoimmune diseases point to the epithelial to mesenchymal transition (EMT) as the common association in the progression of these diseases characterized by an intense inflammatory response. EMT, a process in which epithelial cells are gradually transformed to mesenchymal cells, is a major contributor to the pathogenesis of fibrosis. Importantly, the chronic inflammatory microenvironment has emerged as a decisive factor in the induction of pathological EMT. Transforming growth factor-β (TGF-β), a multifunctional cytokine, plays a crucial role in the induction of fibrosis, often associated with chronic phases of inflammatory diseases, contributing to marked fibrotic changes that severely impair normal tissue architecture and function. The understanding of molecular mechanisms underlying EMT-dependent fibrosis has both a basic and a translational relevance, since it may be useful to design therapies aimed at counteracting organ deterioration and failure. To this end, we reviewed the recent literature to better elucidate the molecular response to inflammatory/fibrogenic signals in autoimmune diseases in order to further the specific regulation of EMT-dependent fibrosis in more targeted therapies.
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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.