Protective Effects of the Soluble Receptor for Advanced Glycation End-Products on Pyroptosis during Myocardial Ischemia-Reperfusion.
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| Abstract |
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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| Authors | Yingming Liu, Xinying Guo, Jie Zhang, Xuejie Han, Hongxia Wang, Fenghe Du, Xiangjun Zeng, Caixia Guo |
| Journal | Oxidative medicine and cellular longevity (Oxid Med Cell Longev) Vol. 2021 Pg. 9570971 ( 2021) ISSN: 1942-0994 [Electronic] United States |
| PMID | 34912499 (Publication Type: Journal Article) |
| Copyright | Copyright © 2021 Yingming Liu et al. |
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