ArticleInternational journal of molecular sciences2022
Relaxin Inhibits the Cardiac Myofibroblast NLRP3 Inflammasome as Part of Its Anti-Fibrotic Actions via the Angiotensin Type 2 and ATP (P2X7) Receptors.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Tumor-derived HMGB2 induces M2-like macrophage polarization via TRIM65-mediated NLRP3 degradation to promote DLBCL progression.Journal for immunotherapy of cancer · 2026Article
- Description of a Large Family with Periodic Fever Carrying a Variant inInternational journal of molecular sciences · 2026Article
- The role of relaxins in blood cell modulation: interactions with relaxin family peptide receptor 1 (RXFP1) and glucocorticoid receptor (GR).Clinical science (London, England : 1979) · 2025Review
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- GPCR dimerization: Drug discovery aspects and targets in renin-angiotensin systems.FASEB bioAdvances · 2025Review
- Relaxin Inhibits Angiotensin II-Induced Cardiac Fibrosis by Activating NO/cGMP Signaling Pathway.Anatolian journal of cardiology · 2025Article
- Review
- AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.Biogerontology · 2024Review
- CircRNA-SCAF8 promotes vascular endothelial cell pyroptosis by regulating the miR-93-5p/TXNIP axis.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Article
- Pyroptosis in renal inflammation and fibrosis: current knowledge and clinical significance.Cell death & disease · 2023Review
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic NLRP3 inflammasome activation can promote fibrosis through its production of interleukin (IL)-1β and IL-18. Conversely, recombinant human relaxin (RLX) can inhibit the pro-fibrotic interactions between IL-1β, IL-18 and transforming growth factor (TGF)-β1. Here, the broader extent by which RLX targeted the myofibroblast NLRP3 inflammasome to mediate its anti-fibrotic effects was elucidated. Primary human cardiac fibroblasts (HCFs), stimulated with TGF-β1 (to promote myofibroblast (HCMF) differentiation), LPS (to prime the NLRP3 inflammasome) and ATP (to activate the NLRP3 inflammasome) (T+L+A) or benzoylbenzoyl-ATP (to activate the ATP receptor; P2X7R) (T+L+Bz), co-expressed relaxin family peptide receptor-1 (RXFP1), the angiotensin II type 2 receptor (AT
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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.