ArticleMolecular and cellular biochemistry2008
Chymase induces profibrotic response via transforming growth factor-beta 1/Smad activation in rat cardiac fibroblasts.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 73 citations in OpenAlex.
- Therapeutic potential, pharmacological role and molecular mechanisms of adelmidrol, an analogue of palmitoylethanolamide.Current research in pharmacology and drug discovery · 2026Review
- The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024Review
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Packaging and Delivery of Asthma Therapeutics.Pharmaceutics · 2021Review
- Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.Medical sciences (Basel, Switzerland) · 2021Review
- Immune regulation of cardiac fibrosis post myocardial infarction.Cellular signalling · 2021Review
- Cardiac Fibrosis: Cellular Effectors, Molecular Pathways, and Exosomal Roles.Frontiers in cardiovascular medicine · 2021Review
- The Histamine 3 Receptor Is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in the Angiotensin II Mouse Model.International journal of molecular sciences · 2020Article
- Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2020Article
- Mast cells and collagen fibrillogenesis.Histochemistry and cell biology · 2020Article
- Review
- Regulation of Cardiac Mast Cell Maturation and Function by the Neurokinin-1 Receptor in the Fibrotic Heart.Scientific reports · 2019Article
- Mast cell-deficiency protects mice from streptozotocin-induced diabetic cardiomyopathy.Translational research : the journal of laboratory and clinical medicine · 2019Article
- Mast Cells in Cardiac Fibrosis: New Insights Suggest Opportunities for Intervention.Frontiers in immunology · 2019Review
- Multifunctional Role of Chymase in Acute and Chronic Tissue Injury and Remodeling.Circulation research · 2018Review
- Mast Cells: Key Contributors to Cardiac Fibrosis.International journal of molecular sciences · 2018Review
- Mast cell chymase promotes hypertrophic scar fibroblast proliferation and collagen synthesis by activating TGF-β1/Smads signaling pathway.Experimental and therapeutic medicine · 2017Article
- Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury.Basic research in cardiology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mast cell-derived chymase is implicated in myocardial fibrosis (MF), but the underlying mechanism of intracellular signaling remains unclear. Transforming growth factor-beta 1 (TGF-beta1) is identified as the most important profibrotic cytokine, and Smad proteins are essential, but not exclusive downstream components of TGF-beta 1 signaling. Moreover, novel evidence indicates that there is a cross talk between Smad and mitogen-activated protein kinase (MAPK) signaling cascade. We investigated whether chymase activated TGF-beta 1/Smad pathway and its potential role in MF by evaluating cardiac fibroblasts (CFs) proliferation and collagen synthesis in neonatal rats. MTT assay and 3H-Proline incorporation revealed that chymase induced CFs proliferation and collagen synthesis in a dose-dependent manner. RT-PCR and Western blot assay demonstrated that chymase not only increased TGF-beta1 expression but also upregulated phosphorylated-Smad2/3 protein. Furthermore, pretreatment with TGF-beta 1 neutralizing antibody suppressed chymase-induced cell growth, collagen production, and Smad activation. In contrast, the blockade of angiotensin II receptor had no effects on chymase-induced production of TGF-beta 1 and profibrotic action. Additionally, the inhibition of MAPK signaling had no effect on Smad activation elicited by chymase. These results suggest that chymase can promote CFs proliferation and collagen synthesis via TGF-beta 1/Smad pathway rather than angiotensin II, which is implicated in the process of MF.
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