Cinnamaldehyde and Nitric Oxide Attenuate Advanced Glycation End Products-Induced the JAK/STAT Signaling in Human Renal Tubular Cells

2015 ◽  
Vol 116 (6) ◽  
pp. 1028-1038 ◽  
Author(s):  
Jau-Shyang Huang ◽  
Ying-Ho Lee ◽  
Lea-Yea Chuang ◽  
Jinn-Yuh Guh ◽  
Jean-Yu Hwang
Keyword(s):  
Nitric Oxide ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Glycation End Products ◽  
End Products ◽  
Stat Signaling ◽  
Renal Tubular

scholarly journals Effects of Nitric Oxide and Antioxidants on Advanced Glycation End Products-Induced Hypertrophic Growth in Human Renal Tubular Cells

2009 ◽  
Vol 111 (1) ◽  
pp. 109-119 ◽  
Author(s):  
Jau-Shyang Huang ◽  
Lea-Yea Chuang ◽  
Jinn-Yuh Guh ◽  
Yann-Jia Huang
Keyword(s):  
Nitric Oxide ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Hypertrophic Growth ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Glycation End Products ◽  
End Products ◽  
Renal Tubular

Advanced glycation end products-mediated hypertrophy is negatively regulated by tetrahydrobiopterin in renal tubular cells

2012 ◽  
Vol 355 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Yi-Chen Liao ◽  
Ying-Ho Lee ◽  
Lea-Yea Chuang ◽  
Jinn-Yuh Guh ◽  
Ming-Der Shi ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Glycation End Products ◽  
End Products ◽  
Renal Tubular

scholarly journals Advanced Glycation End Products Stimulate Angiotensinogen Production in Renal Proximal Tubular Cells

2019 ◽  
Vol 357 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Joseph M. Garagliano ◽  
Akemi Katsurada ◽  
Kayoko Miyata ◽  
Andrei V. Derbenev ◽  
Andrea Zsombok ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Glycation End Products ◽  
End Products ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

scholarly journals Soluble receptor for advanced glycation end products protects from ischemia- and reperfusion-induced acute kidney injury

Biology Open ◽  
2021 ◽  
Author(s):  
Taro Miyagawa ◽  
Yasunori Iwata ◽  
Megumi Oshima ◽  
Hisayuki Ogura ◽  
Koichi Sato ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Advanced Glycation End Products ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Advanced Glycation ◽  
Renal Tubular Damage ◽  
Glycation End Products ◽  
End Products ◽  
Renal Tubular

The full-length receptor for advanced glycation end products (RAGE) is a multiligand pattern recognition receptor. High-mobility group box 1 (HMGB1) is a RAGE ligand of damage-associated molecular patterns that elicits inflammatory reactions. The shedded isoform of RAGE and endogenous secretory RAGE (esRAGE), a splice variant, are soluble isoforms (sRAGE) that act as organ-protective decoys. However, the pathophysiologic roles of RAGE/sRAGE in acute kidney injury (AKI) remain unclear. We found that AKI was more severe, with enhanced renal tubular damage, macrophage infiltration, and fibrosis, in mice lacking both RAGE and sRAGE than in wild-type control mice. Using murine tubular epithelial cells (TECs), we demonstrated that hypoxia upregulated messenger RNA (mRNA) expression of HMGB1 and tumor necrosis factor α (TNF-α), whereas RAGE and esRAGE expressions were paradoxically decreased. Moreover, the addition of recombinant sRAGE canceled hypoxia-induced inflammation and promoted cell viability in cultured TECs. sRAGE administration prevented renal tubular damage in models of ischemia/reperfusion-induced AKI and of anti-glomerular basement membrane (anti-GBM) glomerulonephritis. These results suggest that sRAGE is a novel therapeutic option for AKI.

scholarly journals Exploring the role of body mass index in relationship of serum nitric oxide and advanced glycation end products in apparently healthy subjects

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213307 ◽  
Author(s):  
Elaheh Foroumandi ◽  
Mohammad Alizadeh ◽  
Sorayya Kheirouri ◽  
Mohammad Asghari Jafarabadi
Keyword(s):  
Nitric Oxide ◽  
Body Mass Index ◽  
Advanced Glycation End Products ◽  
Healthy Subjects ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Relationship Of ◽  
Apparently Healthy

Advanced glycation end products induce death of retinal neurons via activation of nitric oxide synthase

2005 ◽  
Vol 81 (6) ◽  
pp. 647-654 ◽  
Author(s):  
Takatoshi Kobayashi ◽  
Hidehiro Oku ◽  
Asako Komori ◽  
Takashi Okuno ◽  
Shota Kojima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Advanced Glycation End Products ◽  
Retinal Neurons ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Oxide Synthase

scholarly journals Advanced glycation end products reduce the calcium transient in cardiomyocytes by increasing production of reactive oxygen species and nitric oxide

FEBS Open Bio ◽  
2017 ◽  
Vol 7 (11) ◽  
pp. 1672-1685 ◽  
Author(s):  
Zeinab Hegab ◽  
Tamer M.A. Mohamed ◽  
Nicholas Stafford ◽  
Mamas Mamas ◽  
Elizabeth J. Cartwright ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Advanced Glycation End Products ◽  
Reactive Oxygen ◽  
Calcium Transient ◽  
Oxygen Species ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Inhibitors of advanced glycation end-products prevent loss of enteric neuronal nitric oxide synthase in diabetic rats

2008 ◽  
Vol 20 (3) ◽  
pp. 253-261 ◽  
Author(s):  
p. v. s. jeyabal ◽  
r. kumar ◽  
p. r. r. gangula ◽  
m.-a. micci ◽  
p. j. pasricha
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Advanced Glycation End Products ◽  
Neuronal Nitric Oxide Synthase ◽  
Diabetic Rats ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Oxide Synthase
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