ArticleOncotarget2017
Relaxin abrogates renal interstitial fibrosis by regulating macrophage polarization via inhibition of Toll-like receptor 4 signaling.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- 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
- Relaxin-2 is a novel biomarker for differentiated thyroid carcinoma in humans.Biochemical pharmacology · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- NLRX1 Prevents M2 Macrophage Polarization and Excessive Renal Fibrosis in Chronic Obstructive Nephropathy.Cells · 2023Article
- Article
- Signaling pathways of chronic kidney diseases, implications for therapeutics.Signal transduction and targeted therapy · 2022Review
- Article
- Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of β-catenin and YAP pathways.Journal of molecular histology · 2021Article
- A relaxin-based nanotherapy for liver fibrosis.Nature nanotechnology · 2021Article
- Mesenchymal Stem Cell-Derived Exosomes Induced by IL-1β Attenuate Urethral Stricture Through Let-7c/PAK1/NF-κB-Regulated Macrophage M2 Polarization.Journal of inflammation research · 2021Article
- Macrophage polarization in innate immune responses contributing to pathogenesis of chronic kidney disease.BMC nephrology · 2020Review
- Relaxin Can Mediate Its Anti-Fibrotic Effects by Targeting the Myofibroblast NLRP3 Inflammasome at the Level of Caspase-1.Frontiers in pharmacology · 2020Article
- AT1R-AT2R-RXFP1 Functional Crosstalk in Myofibroblasts: Impact on the Therapeutic Targeting of Renal and Cardiac Fibrosis.Journal of the American Society of Nephrology : JASN · 2019Article
- Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways.Molecular and cellular endocrinology · 2019Review
- AKF-PD alleviates diabetic nephropathy via blocking the RAGE/AGEs/NOX and PKC/NOX Pathways.Scientific reports · 2019Article
- The Impact of Versatile Macrophage Functions on Acute Kidney Injury and Its Outcomes.Frontiers in physiology · 2019Article
- Empagliflozin, SGLTNaunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Heart Disease and Relaxin: New Actions for an Old Hormone.Trends in endocrinology and metabolism: TEM · 2018Review
- Celastrol treatment protects against acute ischemic stroke-induced brain injury by promoting an IL-33/ST2 axis-mediated microglia/macrophage M2 polarization.Journal of neuroinflammation · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis is a common feature of chronic kidney disease (CKD). To inhibit the CKD process, it is important to prevent renal fibrosis, though CKD remains incurable. Renal fibrosis can be inhibited by relaxin in several experimental models, but the mechanism of relaxin for antifibrotic potential is still not clear. And here we have studied the role of relaxin in macrophage polarization and renal inflammation after unilateral ureteral obstruction (UUO). Our results show that relaxin can downregulate the Toll-like receptor (TLR) 4 signaling, shift macrophage polarization toward the M2 phenotype and ameliorat renal fibrosis in the early stages of UUO. In vitro experiments, it has been confirmed that relaxin can downregulate the TLR4 signaling and induce the M2 macrophage transition. Furthermore, the transitional actions of macrophage phenotype induced by relaxin are significantly blocked by TAK-242, a TLR4 antagonist, in vitro experiments. Thus, there is a novel mechanism of relaxin for antifibrosis that shifts macrophage polarization toward the M2 phenotype via inhibition of TLR4 signaling.
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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.