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Synbindin Downregulation Participates in Slit Diaphragm Dysfunction
Conclusion: Synbindin participates in maintaining foot processes and slit diaphragm as a downstream molecule of SV2B-mediated vesicle transport. Synbindin downregulation participates in slit diaphragm dysfunction. Synbindin can be an early marker to detect podocyte injury.Am J Nephrol
Source: American Journal of Nephrology - August 25, 2021 Category: Neurology Source Type: research

AGE-Induced Suppression of EZH2 Mediates Injury of Podocytes by Reducing H3K27me3
Conclusions: Our studies provide a novel pathway how AGEs contribute to podocyte injury and the formation of the so-called metabolic memory in DKD.Am J Nephrol
Source: American Journal of Nephrology - August 27, 2020 Category: Neurology Source Type: research

Loss of the Golgi Matrix Protein 130 Cause Aberrant IgA1 Glycosylation in IgA Nephropathy
Conclusion: We identified and demonstrated that GM130 plays an important role in IgA1 O-glycans deficiency in IgAN patients, by negatively  regulating C1GALT1 expression. We believe that this finding will provide theoretical foundations for a new mechanism of Gd-IgA1 production in IgAN patients.Am J Nephrol 2019;49:307 –316
Source: American Journal of Nephrology - March 31, 2019 Category: Neurology Source Type: research

Mammalian Target of Rapamycin Complex 1 Activation Disrupts the Low-Density Lipoprotein Receptor Pathway: A Novel Mechanism for Extracellular Matrix Accumulation in Human Peritoneal Mesothelial Cells
Peritoneal fibrosis (PF) is characterized by progressive extracellular matrix (ECM) accumulation. Increasing evidence has suggested that ECM synthesis was increased in human peritoneal mesothelial cells (HPMCs) under high-glucose conditions, but the effects of high-glucose peritoneal dialysis solution (PDS) on ECM synthesis have not been fully elucidated. The aim of this study was to explore the potential mechanisms of high-glucose PDS-induced production of ECM in  HPMCs. HPMCs were stimulated by high-glucose PDS. The activity of mammalian target of rapamycin complex 1 (mTORC1) was inhibited by rapamycin or regulatory-as...
Source: American Journal of Nephrology - November 13, 2018 Category: Neurology Source Type: research

High Uric Acid-Induced Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells via the TLR4/NF-kB Signaling Pathway
Conclusions: UA can induce EMT in renal tubular epithelial cells by the activation of the TLR4/NF- κB signaling pathway, and the targeted intervention of the TLR4/NF-κB signaling pathway might effectively inhibit UA-induced renal interstitial fibrosis mediated by EMT.Am J Nephrol 2017;46:333 –342
Source: American Journal of Nephrology - October 25, 2017 Category: Neurology Source Type: research

Regulation of IgA Class Switch Recombination in Immunoglobulin A Nephropathy: Retinoic Acid Signaling and BATF
Conclusion: These data point toward the role of RA signaling together with BATF in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with neoantigen results in impaired mucosal and systemic IgA responses.Am J Nephrol 2016;43:179-194
Source: American Journal of Nephrology - April 13, 2016 Category: Neurology Source Type: research

Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis
Conclusion: These data points toward the role of TLR3/BAFF axis in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with virus infection results in impaired mucosal and systemic IgA responses.Am J Nephrol 2015;42:185-197
Source: American Journal of Nephrology - September 30, 2015 Category: Neurology Source Type: research

HMGB1 Enhances the AGE-Induced Expression of CTGF and TGF-β via RAGE-Dependent Signaling in Renal Tubular Epithelial Cells
Conclusion: Our results indicated that AGEs induced HMGB-1 and promoted the CTGF and TGF-β in renal epithelial HK-2 cells RAGE-dependently. And there was a synergism between AGEs and HMGB1 in the RAGE signaling activation. The in vitro data suggested that the AGE-RAGE and HMGB-1-RAGE signaling might play an important role in the promotion of CTGF and TGF-β in the renal fibrosis process of diabetic nephropathy.Am J Nephrol 2015;41:257-266
Source: American Journal of Nephrology - April 27, 2015 Category: Neurology Source Type: research