ArticleFrontiers in pharmacology2020
Relaxin Can Mediate Its Anti-Fibrotic Effects by Targeting the Myofibroblast NLRP3 Inflammasome at the Level of Caspase-1.
Article in Frontiers in pharmacology, 2020. 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, 33 citations in OpenAlex.
- Inflammation suppressing activity of jellyfish toxin-derived peptide via downregulation of ROS/NF-κB/NLRP3 signaling in LPS/MSU induced fibroblasts in vitro and in vivo gouty arthritis model.Inflammopharmacology · 2026Article
- Hypertriglyceridemia in chronic kidney disease: pathophysiological mechanisms, cardiovascular risk, and emerging therapeutics.Lipids in health and disease · 2026Review
- Transient angiotensin-converting enzyme inhibition confers sex-specific protection against angiotensin II-induced cardiac remodeling.American journal of physiology. Cell physiology · 2025Article
- Article
- Comprehensive proteomic characterization of urethral stricture disease in the Chinese population.Frontiers in molecular biosciences · 2024Article
- The role of immunosuppressive myofibroblasts in the aging process and age-related diseases.Journal of molecular medicine (Berlin, Germany) · 2023Review
- A Lipidated Single-B-Chain Derivative of Relaxin Exhibits Improved In Vitro Serum Stability without Altering Activity.International journal of molecular sciences · 2023Article
- Anti-inflammatory and anti-fibrotic effects of berberine-loaded liquid crystalline nanoparticles.EXCLI journal · 2023Article
- Relaxin Affects Airway Remodeling Genes Expression through Various Signal Pathways Connected with Transcription Factors.International journal of molecular sciences · 2022Article
- Relaxin Inhibits the Cardiac Myofibroblast NLRP3 Inflammasome as Part of Its Anti-Fibrotic Actions via the Angiotensin Type 2 and ATP (P2X7) Receptors.International journal of molecular sciences · 2022Article
- Role of Inflammasomes in Keloids and Hypertrophic Scars-Lessons Learned from Chronic Diabetic Wounds and Skin Fibrosis.International journal of molecular sciences · 2022Review
- The Scientific Rationale for the Introduction of Renalase in the Concept of Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2022Review
- Cardiac Gene Therapy With Relaxin Receptor 1 Overexpression Protects Against Acute Myocardial Infarction.JACC. Basic to translational science · 2022Article
- The Crucial Role of NLRP3 Inflammasome in Viral Infection-Associated Fibrosing Interstitial Lung Diseases.International journal of molecular sciences · 2021Review
- The Improvement Effect of Sodium Ferulate on the Formation of Pulmonary Fibrosis in Silicosis Mice Through the Neutrophil Alkaline Phosphatase 3 (NALP3)/Transforming Growth Factor-β1 (TGF-β1)/α-Smooth Muscle Actin (α-SMA) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Adapting the Scar-in-a-Jar to Skin Fibrosis and Screening Traditional and Contemporary Anti-Fibrotic Therapies.Frontiers in bioengineering and biotechnology · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe NLRP3 inflammasome produces interleukin (IL)-1β and IL-18, which when chronically activated by transforming growth factor (TGF)-β1, contribute to fibrosis. The recombinant form of the anti-fibrotic hormone, relaxin (RLX), suppresses the pro-fibrotic influence of TGF-β1 and toll-like receptor (TLR)-4 on NLRP3 inflammasome priming and activity in human cardiac myofibroblasts and mice with cardiomyopathy. However, whether RLX also modulates components of the myofibroblast NLRP3 inflammasome remains unknown. METHODS AND
resultsStimulation of a human dermal fibroblast (HDF) cell line with TGF-β1 [5 ng/ml; to promote myofibroblast (HDMF) differentiation], LPS (100 ng/ml; to prime the NLRP3 inflammasome) and ATP (5 mM; to activate the NLPR3 inflammasome) (T+L+A) significantly increased NLRP3 inflammasome priming and activity after 8 and 72 h; and α-SMA expression (myofibroblast differentiation) and collagen-I deposition after 72 h. siRNA-induced knock-down of NLRP3 inflammasome priming components (NLRP3, ASC, caspase-1) in T+L+A-stimulated HDMFs for 24 h, completely knocked-down each component after 72 h. RLX (100 ng/ml) administration to T+L+A-stimulated HDMFs after control, NLRP3 or ASC siRNA transfection, equivalently suppressed IL-1β, pro-IL-18, α-SMA, and collagen-I protein levels (by 40%-50%; all p<0.05 vs. T+L+A) after 72 h, as determined by Western blotting. These RLX-induced effects were abrogated by siRNA knock-down of caspase-1.
conclusionThe anti-fibrotic actions of RLX appear to require modulation of caspase-1 within the myofibroblast NLRP3 inflammasome.
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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 OpenQuestion graph.