ArticleBioengineered2021
Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/ transforming growth factor-β (TGF-β1)/Smad axis.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Hepatocyte-Derived S100A4/A6/A10/A11 Proteins Promote Liver Fibrosis by Direct and Indirect Activation of HSCs.Inflammation · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Comparative analysis of S100A10 and S100A11 in MASLD and hepatic cancer development revealed a tumor suppressive role for S100A10.Cell death & disease · 2025Article
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Dual inhibition of TGFβ and PDGF improves RV remodeling and function in response to RV pressure or volume-loading.Physiological reports · 2025Article
- Morroniside improves AngII-induced cardiac fibroblast proliferation, migration, and extracellular matrix deposition by blocking p38/JNK signaling pathway through the downregulation of KLF5.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Unlocking the potential of tranilast: Targeting fibrotic signaling pathways for therapeutic benefit.International immunopharmacology · 2024Review
- Fosinopril inhibits Ang II-induced VSMC proliferation, phenotype transformation, migration, and oxidative stress through the TGF-β1/Smad signaling pathway.Open life sciences · 2024Article
- Myriad factors and pathways influencing tumor radiotherapy resistance.Open life sciences · 2024Review
- Resveratrol plays an anti-fibrotic and anti-autophagy role by stimulating miR-192-5p expression in urethral fibrosis.Functional & integrative genomics · 2023Article
- Biomimetic Electrospun Scaffold-Based In Vitro Model Resembling the Hallmarks of Human Myocardial Fibrotic Tissue.ACS biomaterials science & engineering · 2023Article
- Levocarnitine regulates the growth of angiotensin II-induced myocardial fibrosis cells via TIMP-1.Open life sciences · 2023Article
- Article
- Transcriptome sequencing and lncRNA-miRNA-mRNA network construction in cardiac fibrosis and heart failure.Bioengineered · 2022Article
- Quantitative proteomics reveal three potential biomarkers for risk assessment of acute myocardial infarction.Bioengineered · 2022Article
- The Role of NLRP3 Inflammasome in Alzheimer's Disease and Potential Therapeutic Targets.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tranilast has an ameliorative effect on myocardial fibrosis (MF), but the specific mechanism has not been studied. S100A11 is a key regulator of collagen expression in MF. In this paper, we will study the regulatory roles of Tranilast and S100A11 in MF. After the introduction of angiotensin II (AngII) to Human cardiac fibroblasts (HCF), Tranilast was administered. CCK-8 kit was used to detect cell viability. Wound Healing assay detected cell migration, and Western blot was used to detect the expression of migration-related proteins and proteins related to extracellular matrix synthesis. The expression of α-SMA was detected by immunofluorescence (IF). The expression of S100A11 was detected by qPCR and Western blot, and then S100A11 was overexpressed by cell transfection technology, so as to explore the mechanism by which Tranilast regulated MF. In addition, the expression of TGF-β1/Smad pathway related proteins was detected by Western blot. Tranilast inhibited Ang II-induced over-proliferation, migration and fibrosis of human cardiac fibroblasts (HCF), and simultaneously significantly decreased S100A11 expression was observed. Overexpression of S100A11 reversed the inhibition of Tranilast on AngII-induced over-proliferation, migration, and fibrosis in HCF, accompanied by activation of the TGF-β1/Smad pathway. Overall, Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/TGF-β1/Smad axis.
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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 Socratic graph.