ArticleInternational journal of molecular sciences2019
Dual Role of Triptolide in Interrupting the NLRP3 Inflammasome Pathway to Attenuate Cardiac Fibrosis.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- A Chinese case series of Schnitzler syndrome and complete remission in one tocilizumab-treated patient.Clinical rheumatology · 2020Pooled it
- Disruption of the Fibroinflammatory Loop: A Therapeutic Strategy for Cardiac Fibrosis in Non-Ischemic Cardiomyopathy.Reviews in cardiovascular medicine · 2026Article
- Quantitative Analysis of Flavonols and Their Glycosides and Gastrointestinal Transformation of Flavonol Glycosides in Yinxing Mihuan Oral Solution.Journal of analytical methods in chemistry · 2026Article
- Advances in targeting myocardial fibrosis: integrating mechanisms and therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Diterpenes: Nature's Hidden Gems of Immunomodulation.International journal of molecular sciences · 2025Review
- PCSK9 Enhances Cardiac Fibrogenesis via the Activation of Toll-like Receptor and NLRP3 Inflammasome Signaling.International journal of molecular sciences · 2025Article
- Triptolide attenuates LPS-induced chondrocyte inflammation by inhibiting inflammasome activation via the Wnt/β-catenin and NF-κB signaling pathways.Cytotechnology · 2025Article
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 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
- Regulated Cell Death Pathways in Pathological Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2024Review
- Plant-Derived Terpenoids: A Plethora of Bioactive Compounds with Several Health Functions and Industrial Applications-A Comprehensive Overview.Molecules (Basel, Switzerland) · 2024Review
- Zebrafish as an innovative model for exploring cardiovascular disease induction mechanisms and novel therapeutic interventions: a molecular insight.Molecular biology reports · 2024Review
- Mitochondria and NLRP3 inflammasome in cardiac hypertrophy.Molecular and cellular biochemistry · 2024Review
- The role of pyroptosis in heart failure and related traditional chinese medicine treatments.Frontiers in pharmacology · 2024Review
- Potential Impact of Bioactive Compounds as NLRP3 Inflammasome Inhibitors: An Update.Current pharmaceutical biotechnology · 2024Review
- Repositioning Glibenclamide in cardiac fibrosis by targeting TGF-β1-pSmad2/3-NLRP3 cascade.Molecular and cellular biochemistry · 2023Article
- Allicin protects against LPS-induced cardiomyocyte injury by activating Nrf2-HO-1 and inhibiting NLRP3 pathways.BMC cardiovascular disorders · 2023Article
- Gefapixant, a Novel P2X3 Antagonist, Protects against Post Myocardial Infarction Cardiac Dysfunction and Remodeling Via Suppressing NLRP3 Inflammasome.Current medical science · 2023Article
- Dehydroisohispanolone as a Promising NLRP3 Inhibitor Agent: Bioevaluation and Molecular Docking.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
In a previous paper, we reported that triptolide (TP), a commonly used immunomodulator, could attenuate cardiac hypertrophy. This present study aimed to further explore the inhibition of cardiac fibrosis by TP and the possible mechanism from the perspective of the NOD-like receptor protein 3 (NLRP3) inflammasome. Hematoxylin-eosin and Masson's staining, immunohistochemistry, and immunofluorescence were performed to observe cardiac fibrotic changes in mice and mouse cardiac fibroblasts (CFs). The Western blot, colocalization, and immunoprecipitation were applied to detect protein expression and interactions. Results suggested that TP dose-dependently inhibited cardiac fibrosis induced by isoproterenol and collagen production of CFs induced by angiotensin II. TP exhibited an antifibrotic effect via inhibiting activation of the NLRP3 inflammasome, which sequentially decreased IL-1β maturation, myeloid differentiation factor 88 (MyD88)-related phosphorylation of c-Jun N-terminal kinase (JNK), extracellular regulated protein kinase 1/2 (ERK1/2), and TGF-β1/Smad signaling, and ultimately resulted in less collagen production. Moreover, TP showed no antifibrotic effect in
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