Relaxin Inhibits High Glucose-Induced Matrix Accumulation in Human Mesangial Cells by Interfering with TGF-β1 Production and Mesangial Cells Phenotypic Transition.

No abstract is available for this paper.

• Publication year

  2015

• Venue

  Biological and Pharmaceutical Bulletin

• Publication date

  2015-10-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1248/bpb.b15-00127PMID 26424011
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Solution structure, aggregation behavior, and flexibility of human relaxin-2.

  2015cited by this paper
• Therapeutic strategies of diabetic nephropathy: recent progress and future perspectives.

  2015cited by this paper
• Novel therapeutic approaches for diabetic nephropathy and retinopathy.

  2015cited by this paper
• The effects of urokinase-type plasminogen activator (uPA) on cell proliferation and phenotypic transformation of rat mesangial cells induced by high glucose.

  2014cited by this paper
• Updates on the Management of Diabetes in Dialysis Patients

  2014cited by this paper
• New Targets for Renal Interstitial Fibrosis: Relaxin Family Peptide Receptor 1 - Angiotensin Type 2 Receptor Heterodimers

  2014cited by this paper
• Role of protein kinase C β2 in relaxin-mediated inhibition of cardiac fibrosis

  2014cited by this paper
• Relaxin: New Pathophysiological Aspects and Pharmacological Perspectives for an Old Protein

  2014cited by this paper
• Role of caveolae in high glucose and TGF-β₁ induced fibronectin production in rat mesangial cells.

  2014cited by this paper
• Relaxin requires the angiotensin II type 2 receptor to abrogate renal interstitial fibrosis.

  2014cited by this paper
• Novel effective drugs for diabetic kidney disease? or not?

  2014cited by this paper
• The pathogenesis of diabetic nephropathy: focus on microRNAs and proteomics.

  2013cited by this paper
• The regulation of fibrosis in airway remodeling in asthma.

  2012cited by this paper
• Up-regulating relaxin expression by G-quadruplex interactive ligand to achieve antifibrotic action.

  2012cited by this paper
• Relaxin ameliorates salt-sensitive hypertension and renal fibrosis.

  2012cited by this paper
• STAT1 mediates cellular senescence induced by angiotensin II and H2O2 in human glomerular mesangial cells

  2011cited by this paper
• Pathologic classification of diabetic nephropathy.

  2010cited by this paper
• Connective tissue growth factor(CCN2), a pathogenic factor in diabetic nephropathy. What does it do? How does it do it?

  2009cited by this paper
• Relaxin inhibits renal myofibroblast differentiation via RXFP1, the nitric oxide pathway, and Smad2

  2009cited by this paper
• [Molecular mechanisms of tissue fibrosis].

  2009cited by this paper
• Effects of Relaxin on Development of Mesangial Proliferative Nephritis

  2009cited by this paper
• Relaxin ameliorates fibrosis in experimental diabetic cardiomyopathy.

  2008cited by this paper
• From Fibrosis to Sclerosis

  2008cited by this paper
• Diabetic Nephropathy: Mechanisms of Renal Disease Progression

  2008cited by this paper
• Regulation of transforming growth factor beta in diabetic nephropathy: implications for treatment.

  2007cited by this paper
• Relaxin in cardiovascular and renal disease.

  2006cited by this paper
• Relaxin Stimulates Multiple Signaling Pathways: Activation of cAMP, PI3K, and PKCζ in THP‐1 Cells

  2005cited by this paper
• The antifibrotic effects of relaxin in human renal fibroblasts are mediated in part by inhibition of the Smad2 pathway.

  2005cited by this paper
• New Insights into Biological Roles of Relaxin and Relaxin-related Peptides

  2005cited by this paper
• Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator.

  2004cited by this paper
• Relaxin's physiological roles and other diverse actions.

  2004cited by this paper
• Mediators of Diabetic Renal Disease: The Case for TGF-β as the Major Mediator

  2004cited by this paper
• Role of TGF-beta signaling in extracellular matrix production under high glucose conditions.

  2003cited by this paper
• Pathogenesis of fibrosis: role of TGF-beta and CTGF.

  2002cited by this paper
• High glucose-enhanced mesangial cell extracellular signal-regulated protein kinase activation and alpha1(IV) collagen expression in response to endothelin-1: role of specific protein kinase C isozymes.

  2001cited by this paper
• Stimulation of TGF-beta type II receptor by high glucose in mouse mesangial cells and in diabetic kidney.

  2000cited by this paper
• Transforming growth factor β contributes to progressive diabetic nephropathy

  2000cited by this paper
• Transforming growth factor beta contributes to progressive diabetic nephropathy.

  2000cited by this paper

• Research on rhubarb's natural components and their potential for treating chronic kidney disease.

  2026cites this paper
• Network pharmacology and molecular docking technology-based predictive study and potential targets analysis of icariin for the treatment of diabetic nephropathy.

  2025cites this paper
• Exploring inflammatory and fibrotic mechanisms driving diabetic nephropathy progression.

  2025cites this paper
• Therapeutic approaches and novel antifibrotic agents in renal fibrosis: A comprehensive review

  2024cites this paper
• Colquhounia root tablet improves diabetic kidney disease by regulating epithelial-mesenchymal transition via the PTEN/PI3K/AKT pathway

  2024cites this paper
• Macrophage polarization in tissue fibrosis

  2023cites this paper
• Cellular phenotypic transitions in diabetic nephropathy: An update

  2022cites this paper
• Prediction of the Potential Mechanism of Triptolide in Improving Diabetic Nephropathy by Utilizing A Network Pharmacology and Molecular Docking Approach.

  2022cites this paper
• Relaxin as an anti-fibrotic treatment: perspectives, challenges and future directions.

  2021cites this paper
• Study of the Active Components and Molecular Mechanism of Tripterygium wilfordii in the Treatment of Diabetic Nephropathy

  2021cites this paper
• Signaling Pathways Involved in Diabetic Renal Fibrosis

  2021cites this paper
• Rhein-8-O-β-D-glucopyranoside inhibited high glucose-induced apoptosis of human mesangial cells by regulating the lincRNA ANRIL/let-7a/TGF-β1/Smad signaling pathway

  2020influential citation
• A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy.

  2019cites this paper
• The Influence of a Nanopatterned Scaffold that Mimics Abnormal Renal Mesangial Matrix on Mesangial Cell Behavior

  2019cites this paper
• Notch pathway mediates podocyte injury and extracellular matrix synthesis in diabetic nephropathy

  2018cites this paper
• Triptolide inhibits lipopolysaccharide-induced proliferation , induces apoptosis and causes cell cycle arrest of human mesangial cells in vitro

  2018cites this paper
• Relaxin Ameliorates Renal Fibrosis and Expression of Endothelial Cell Transition Markers in Rats of Isoproterenol-Induced Heart Failure.

  2017cites this paper
• Mori cortex prevents kidney damage through inhibiting expression of inflammatory factors in the glomerulus in streptozocin-induced diabetic rats

  2017cites this paper
• Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice

  2017cites this paper
• Protective effects and microarray-based mechanism of sea cucumber hydrolysates against high-glucose induced nephrotoxicity in mouse glomerulus mesangial cells

  year unknowncites this paper