The role of iNKT cells and receptors for advanced glycation end products (RAGE) in lung ischemia-reperfusion injury

2012 ◽  
Author(s):  
Ashish Kumar Sharma
Keyword(s):  
Reperfusion Injury ◽  
Advanced Glycation End Products ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Advanced Glycation ◽  
Inkt Cells ◽  
Glycation End Products ◽  
End Products

scholarly journals Protective Effects of the Soluble Receptor for Advanced Glycation End-Products on Pyroptosis during Myocardial Ischemia-Reperfusion

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yingming Liu ◽  
Xinying Guo ◽  
Jie Zhang ◽  
Xuejie Han ◽  
Hongxia Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Advanced Glycation End Products ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Soluble Receptor ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Myocardial Ischemia Reperfusion

Ischemia-reperfusion injury (IRI) is an inevitable process when reperfusion therapy undergoes in acute myocardial infarction patients, which will lead to cardiac cell death. Many factors have been found to protect the myocardium, one of which was the soluble receptor for advanced glycation end-products (sRAGE) that protected the myocardium from apoptosis and autophagy. However, pyroptosis is also an important form of cell death that occurs during ischemia-reperfusion (I/R), whose critical molecule, NLR family pyrin domain containing 3 (NLRP3), was ever reported to be inhibited by sRAGE; therefore, it is hypothesized that sRAGE may decrease the cardiac pyroptosis induced by I/R. The results showed that sRAGE protected cardiomyocytes from I/R-induced pyroptosis by decreasing the expression level of NLRP3, gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18). Meanwhile, the results from primary cultured cardiomyocytes showed that the NF-κB pathway mediated the effects of sRAGE on pyroptosis. Therefore, it is concluded that sRAGE protects the heart from pyroptosis through inhibiting the NF-κB pathway during myocardial ischemia-reperfusion.

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