ReviewJHEP reports : innovation in hepatology2022
Transforming growth factor β latency: A mechanism of cytokine storage and signalling regulation in liver homeostasis and disease.
Review in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
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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.
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Who cites it
57 citing papers in PubMed, 74 citations in OpenAlex.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- DietaryGenes · 2026Article
- The instructive scar - the dynamic role of extracellular matrix in biliary pathophysiology.Disease models & mechanisms · 2026Review
- Extracellular matrix and proteolysis: mechanisms driving irreversible changes and shaping cell behavior.The FEBS journal · 2026Review
- Mesangial Cell-Derived Extracellular Matrix Protein 1 Is Essential for Maintaining Mesangial Matrix Homeostasis and Glomerular Architecture.Journal of the American Society of Nephrology : JASN · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Targeted Therapy and Immunotherapies in Hepatocellular Carcinoma: Mechanisms and Clinical Studies.MedComm · 2026Review
- Fibrosis suppressive effect and mechanism of CaSR positive allosteric modulators/p-dioxanone copolymers.Drug delivery and translational research · 2026Article
- CircATXN2 exacerbates pulmonary arterial hypertension by modulating the miR-138-5p/SMURF1 axis.Respiratory research · 2026Article
- Article
- ECM1 produced by hepatic stellate cells serves as a gatekeeper of liver homeostasis in hepatic fibrosis.Hepatology (Baltimore, Md.) · 2026Article
- Article
- [Cajanonic acid A derivative XJ-60 improves liver fibrosis in mice with non-alcoholic fatty liver disease by inhibiting the SP1/TGF-β/Smad3 signaling axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- Review
- Melandryoside attenuates steatohepatitis and fibrosis by restoring PPM1A-mediated SMAD signaling termination.Frontiers in pharmacology · 2026Article
- Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease: A Multicellular Perspective.The American journal of pathology · 2026Review
- Determining the salivary levels of Transforming Growth Factor Beta 1 (TGF-β1) and Vascular Endothelial Growth Factor (VEGF) during the three stages of orthodontic treatment in patients in Mangaluru: A prospective study.Journal of orthodontic science · 2026Article
- Cell networks in the mouse liver during partial hepatectomy.Stem cell reports · 2025Article
- Persistent tissue regeneration and transforming growth factor-β induced fibrosis in the masseter muscle of mdxScientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β) is a potent effector in the liver, which is involved in a plethora of processes initiated upon liver injury. TGF-β affects parenchymal, non-parenchymal, and inflammatory cells in a highly context-dependent manner. Its bioavailability is critical for a fast response to various insults. In the liver - and probably in other organs - this is made possible by the deposition of a large portion of TGF-β in the extracellular matrix as an inactivated precursor form termed latent TGF-β (L-TGF-β). Several matrisomal proteins participate in matrix deposition, latent complex stabilisation, and activation of L-TGF-β. Extracellular matrix protein 1 (ECM1) was recently identified as a critical factor in maintaining the latency of deposited L-TGF-β in the healthy liver. Indeed, its depletion causes spontaneous TGF-β signalling activation with deleterious effects on liver architecture and function. This review article presents the current knowledge on intracellular L-TGF-β complex formation, secretion, matrix deposition, and activation and describes the proteins and processes involved. Further, we emphasise the therapeutic potential of toning down L-TGF-β activation in liver fibrosis and liver cancer.
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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.