Advanced glycation end-products suppress autophagy by AMPK/mTOR signaling pathway to promote vascular calcification

2020 ◽  
Vol 471 (1-2) ◽  
pp. 91-100 ◽  
Author(s):  
Yanyan Liu ◽  
Jing Li ◽  
Yuting Han ◽  
Yuying Chen ◽  
Lixuan Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Vascular Calcification ◽  
Advanced Glycation End Products ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Advanced glycation end products increase endothelial permeability through the RAGE/Rho signaling pathway

FEBS Letters ◽  
2009 ◽  
Vol 584 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Akiko Hirose ◽  
Takahisa Tanikawa ◽  
Hiroko Mori ◽  
Yosuke Okada ◽  
Yoshiya Tanaka
Keyword(s):  
Signaling Pathway ◽  
Advanced Glycation End Products ◽  
Endothelial Permeability ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Receptor for advanced glycation end products: a key molecule in the genesis of chronic kidney disease vascular calcification and a potential modulator of sodium phosphate co-transporter PIT-1 expression

2019 ◽  
Vol 34 (12) ◽  
pp. 2018-2030 ◽  
Author(s):  
Karim Belmokhtar ◽  
Jeremy Ortillon ◽  
Stéphane Jaisson ◽  
Ziad A Massy ◽  
Camille Boulagnon Rombi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Advanced Glycation End Products ◽  
Mrna Levels ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
High Phosphate

Abstract Background Chronic kidney disease (CKD) is associated with increased cardiovascular mortality, frequent vascular calcification (VC) and accumulation of uraemic toxins. Advanced glycation end products and S100 proteins interact with the receptor for advanced glycation end products (RAGE). In the present work, we aimed to investigate the role(s) of RAGE in the CKD–VC process. Methods Apoe−/− or Apoe−/−Ager (RAGE)−/− male mice were assigned to CKD or sham-operated groups. A high-phosphate diet was given to a subgroup of Apoe−/−and Apoe−/−Ager−/− CKD mice. Primary cultures of Ager+/+ and Ager−/− vascular smooth muscle cells (VSMCs) were established and stimulated with either vehicle, inorganic phosphate (Pi) or RAGE ligands (S100A12; 20 µM). Results After 12 weeks of CKD we observed a significant increase in RAGE ligand (AGE and S100 proteins) concentrations in the serum of CKD Apoe−/− mice. Ager messenger RNA (mRNA) levels were 4-fold higher in CKD vessels of Apoe−/− mice. CKD Apoe−/− but not CKD Apoe−/− or Ager−/− mice displayed a marked increase in the VC surface area. Similar trends were found in the high-phosphate diet condition. mRNA levels of Runx2 significantly increased in the Apoe−/− CKD group. In vitro, stimulation of Ager+/+VSMCs with Pi or S100A12 induced mineralization and osteoblast transformation, and this was inhibited by phosphonoformic acid (Pi co-transporters inhibitor) and Ager deletion. In vivo and in vitro RAGE was necessary for regulation of the expression of Pit-1, at least in part through production of reactive oxygen species. Conclusion RAGE, through the modulation of Pit-1 expression, is a key molecule in the genesis of VC.

scholarly journals Reduction of Advanced-Glycation End Products Levels and Inhibition of RAGE Signaling Decreases Rat Vascular Calcification Induced by Diabetes

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85922 ◽  
Author(s):  
Mathieu R. Brodeur ◽  
Céline Bouvet ◽  
Sonia Bouchard ◽  
Simon Moreau ◽  
Jeanne Leblond ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products
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