ArticleFrontiers in physiology2016
Essential Role of Lyn in Fibrosis.
Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Unveiling the Immunopharmacological Mechanisms of Biejiajian Pills (BJJP) Underlying the Treatment of Hepatic Fibrosis: Insights From Network Pharmacology and Experimental Validation.Food science & nutrition · 2026Article
- Proteomic and Functional Comparison of Extracellular Vesicles from Wild-Type and Lyn-Deficient Stromal Cells.Advances in experimental medicine and biology · 2026Article
- Fibrosis in Chronic Kidney Disease: Pathophysiology and Therapeutic Targets.Journal of clinical medicine · 2024Review
- LYN kinase programs stromal fibroblasts to facilitate leukemic survival via regulation of c-JUN and THBS1.Nature communications · 2023Article
- Intimate intertwining of the pathogenesis of hypoxia and systemic sclerosis: A transcriptome integration analysis.Frontiers in immunology · 2022Article
- ACLY is the novel signaling target of PIPHeliyon · 2020Article
- Lyn Kinase Promotes the Proliferation of Malignant Melanoma Cells through Inhibition of Apoptosis and Autophagy via the PI3K/Akt Signaling Pathway.Journal of Cancer · 2019Article
- Adhesion structures in leukemia cells and their regulation by Src family kinases.Cell adhesion & migration · 2018Article
- Src family kinases in chronic kidney disease.American journal of physiology. Renal physiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Fibrotic disorders involve replacement of normal parenchyma with myofibroblasts, which deposit connective tissue, leading to obliteration of the function of the underlying organ. The treatment options are inadequate and reflect the fact that signaling targets in myofibroblasts are unknown. Here we identify the hyperactive Lyn signaling in myofibroblasts of patients with chronic pancreatitis-induced fibrosis. Lyn activation coexpress with markers of activated myofibroblasts, and is increased ~11-fold in chronic pancreatitis compared to normal tissue. Inhibition of Lyn with siRNA or INNO-406 leads to the substantial decrease of migration and proliferation of human chronic pancreatitis myofibroblasts in vitro, while leaving migration and proliferation of normal myofibroblasts only slightly affected. Furthermore, inhibition of Lyn prevents synthesis of procollagen and collagen in myofibroblasts in a mouse model of chronic pancreatitis-induced fibrosis. We conclude that Lyn, as a positive regulator of myofibroblast migration, proliferation, and collagen production, is a key target for preventing fibrosis.
Indexed as
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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.