ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2015
Novel insights into the function and dynamics of extracellular matrix in liver fibrosis.
Review in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.
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
144 citing papers in PubMed, 1 synthesis or guideline pooled it, 266 citations in OpenAlex.
- High throughput interrogation of human liver stellate cells reveals microenvironmental regulation of phenotype.Acta biomaterialia · 2022Pooled it
- Endotrophin is a risk marker of complications in CANagliflozin cardioVascular Assessment Study (CANVAS): a randomized controlled trial.Cardiovascular diabetology · 2022Trial
- Serum endotrophin identifies optimal responders to PPARγ agonists in type 2 diabetes.Diabetologia · 2017Trial
- Role of extracellular matrix in liver fibrosis regression and regeneration (Review).International journal of molecular medicine · 2026Review
- DietaryGenes · 2026Article
- In Vitro Assessment of Nintedanib in Keratoconus Corneal Stromal Microenvironment.Biomolecules · 2026Article
- Article
- The Regulatory Role of Iron Transporter SLC39A13 in Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fibrosis activityJHEP reports : innovation in hepatology · 2026Article
- Fatty liver regeneration after partial hepatectomy: an experimental study based on intravoxel incoherent motion and T2Magma (New York, N.Y.) · 2026Article
- Spatial patterning strategies for liver tissue engineering: Biofabrication technologies and applications.Advanced drug delivery reviews · 2026Review
- Regulation of Tissue Regeneration by Immune Microenvironment-Fibroblast Interactions.International journal of molecular sciences · 2025Review
- Growing Pains: GH-induced Fibrosis Across Multiple Organs in bGH Mice.Endocrinology · 2025Article
- Signatures of proteomics and glycoproteomics revealed liraglutide ameliorates MASLD by regulating specific metabolic homeostasis in mice.Journal of pharmaceutical analysis · 2025Article
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- The role of tetraspanins in organ fibrosis: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- Endothelial histone deacetylase 9 promotes diabetic retinopathy in mice by regulating endothelial-mesenchymal transition.Acta pharmacologica Sinica · 2025Article
- ECM formation and degradation during fibrosis, repair, and regeneration.npj metabolic health and disease · 2025Review
- Organ fibrosis: beyond collagen I expression. Fibroblast phenotype and basement membrane proteins.American journal of physiology. Cell physiology · 2025Review
- A Robust Expression and Purification Protocol for the Production of the La Domain of Human LARP6.ACS omega · 2025Article
84 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
14 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that altered components and posttranslational modifications of proteins in the extracellular matrix (ECM) may both initiate and drive disease progression. The ECM is a complex grid consisting of multiple proteins, most of which play a vital role in containing the essential information needed for maintenance of a sophisticated structure anchoring the cells and sustaining normal function of tissues. Therefore, the matrix itself may be considered as a paracrine/endocrine entity, with more complex functions than previously appreciated. The aims of this review are to 1) explore key structural and functional components of the ECM as exemplified by monogenetic disorders leading to severe pathologies, 2) discuss selected pathological posttranslational modifications of ECM proteins resulting in altered functional (signaling) properties from the original structural proteins, and 3) discuss how these findings support the novel concept that an increasing number of components of the ECM harbor signaling functions that can modulate fibrotic liver disease. The ECM entails functions in addition to anchoring cells and modulating their migratory behavior. Key ECM components and their posttranslational modifications often harbor multiple domains with different signaling potential, in particular when modified during inflammation or wound healing. This signaling by the ECM should be considered a paracrine/endocrine function, as it affects cell phenotype, function, fate, and finally tissue homeostasis. These properties should be exploited to establish novel biochemical markers and antifibrotic treatment strategies for liver fibrosis as well as other fibrotic diseases.
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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.