Protective Effects of the Soluble Receptor for Advanced Glycation End-Products on Pyroptosis during Myocardial Ischemia-Reperfusion.
Protective Effects of the Soluble Receptor for Advanced Glycation End-Products on Pyroptosis during Myocardial Ischemia-Reperfusion.
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晚期糖基化终产物可溶性受体对心肌缺血再灌注过程中细胞焦亡的保护作用
DOI：
10.1155/2021/9570971
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发表时间：
2021
影响因子：
--
通讯作者：
Guo C
中科院分区：
文献类型：
--
作者：
Liu Y;Guo X;Zhang J;Han X;Wang H;Du F;Zeng X;Guo C
缺血再灌注损伤(IRI)是急性心肌梗死患者在接受再灌注治疗时不可避免的过程，它会导致心肌细胞死亡。已发现许多保护心肌的因素，其中之一是晚期糖基化终产物的可溶性受体(SRAGE)，它保护心肌免受细胞凋亡和自噬的影响。然而，SRAGE也是缺血再灌注(I/R)时细胞死亡的一种重要形式，其关键分子NLRP3家族结构域(NLRP3)曾被SRAGE抑制，因此推测SRAGE可减轻I/R所致的心脏下垂。结果表明，SRAGE通过降低NLRP3、Gasdermin D(GSDMD)、IL-1β(IL-1β)和IL-18(IL-18)的表达水平，对心肌细胞具有保护作用。同时，原代培养的心肌细胞的实验结果表明，NF-κB通路介导了sRAGE治疗下垂的作用。结论：sRAGE通过抑制心肌缺血再灌流过程中的NF-κB通路，保护心脏免受重度下垂的影响。
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.