ArticleJournal of molecular histology2018
NLRP1 promotes TGF-β1-induced myofibroblast differentiation in neonatal rat cardiac fibroblasts.
Article in Journal of molecular histology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Antibody-conjugated SIS3-loaded PLGA@polydopamine nanoparticles alleviate cardiac fibrosis by modulating Smad3 signaling in myofibroblasts.Journal of nanobiotechnology · 2026Article
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- Cardiac hypertrophy that affects hyperthyroidism occurs independently of the NLRP3 inflammasome.Pflugers Archiv : European journal of physiology · 2024Article
- Sirt1 Inhibits Atrial Fibrosis by Downregulating the Expression of the Transforming Growth Factor-β1/Smad Pathway.Acta Cardiologica Sinica · 2024Article
- The Relationship between the Serum NLRP1 Level and Coronary Lesions in Patients with Coronary Artery Disease.International journal of clinical practice · 2023Article
- The Mechanism and Regulation of the NLRP3 Inflammasome during Fibrosis.Biomolecules · 2022Review
- Lysine demethylase 3A is a positive regulator of cardiac myofibroblast transdifferentiation that increases Smad3 phosphorylation following transforming growth factor beta1 stimulation.Molecular biology reports · 2022Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- Long noncoding RNA H19 suppresses cardiac hypertrophy through the MicroRNA-145-3p/SMAD4 axis.Bioengineered · 2022Article
- MiR-375-3p Promotes Cardiac Fibrosis by Regulating the Ferroptosis Mediated by GPX4.Computational intelligence and neuroscience · 2022Article
- The mapping of mRNA alterations elucidates the etiology of radiation-induced pulmonary fibrosis.Frontiers in genetics · 2022Article
- TRIM25 Rescues Against Doxorubicin-Induced Pyroptosis Through Promoting NLRP1 Ubiquitination.Cardiovascular toxicology · 2021Article
- Inflammasomes and Fibrosis.Frontiers in immunology · 2021Review
- The Role of the Inflammasome in Heart Failure.Frontiers in physiology · 2021Review
- hUMSCs regulate the differentiation of ovarian stromal cells via TGF-βStem cell research & therapy · 2020Article
- [Expression of NLRP1 inflammasomes in myocardial tissue of diabetic rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear localization leucine-rich-repeat protein 1 (NLRP1) is a member of Nod-like receptors (NLRs) family. Recent studies have reported that NLRP1 is involved in various diseases, especially in cardiovascular diseases. However, the effect of NLRP1 on cardiac fibrosis remains unclear. In this study, NLRP1 overexpression and NLRP1 silencing constructs were transfected into neonatal rat cardiac fibroblasts induced by TGF-β1 for 48 h to investigate the effect of NLRP1 in cardiac fibrosis and its molecular mechanisms. Cardiac fibroblasts were transfected with NLRP1 and then cultured in the presence and absence of TGF-β1and Smad3 inhibitor (SIS3). Our data indicated that NLRP1 not only promoted fibroblast activation and myofibroblast differentiation, but also upregulated the mRNA and protein levels of α-SMA in the TGF-β1-treated neonatal rat cardiac fibroblasts. Overexpressing NLRP1 in TGF-β1-induced cardiac fibroblasts upregulated the mRNA and protein levels of Collagen I, Collagen III, and connective tissue growth factor. Moreover, NLRP1 upregulated the protein levels of Smad2, Smad3, and Smad4 in nuclei of fibroblasts, and attenuated levels of phosphorylated Smad2 and Smad3 in the cytoplasm of fibroblasts induced by TGF-β1. In addition, the increase in fibrotic genes and Smad proteins was significantly reduced in the presence of SIS3. Our findings illustrated that NLRP1 promoted myofibroblast differentiation and excessive ECM production in TGF-β1-induced neonatal cardiac fibroblasts through directly targeting TGF-β1/Smad signaling pathways.
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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.