Arrhythmia Center, Ningbo First Hospital, Ningbo, Zhejiang, China.
J Recept Signal Transduct Res. 2021 Feb;41(1):32-37. doi: 10.1080/10799893.2020.1783682. Epub 2020 Jun 24.
Necroptosis is a new type of cell death. However, the role of necroptosis in LPS-related cardiomyocyte damage has not been fully understood. The aim of our study is to explore the molecular mechanism underlying inflammation-mediated cardiomyocyte necroptosis. H9C2 cardiomyocyte cell line was treated with LPS. Then, cell viability and necroptosis were measured through qPCR and ELISA. Pathway analysis was performed to verify whether Ripk3/Pgam5 signaling pathway is implicated into the regulation of cardiomyocyte necroptosis. The results demonstrated that LPS reduced cardiomyocyte viability and activated necroptosis. At the molecular levels, oxidative stress and inflammation were triggered by LPS and these alterations may contribute to the activation of necroptosis. Finally, we found that Ripk3/Pgam5 signaling pathway was activated by LPS in cardiomyocyte and this signaling pathway may explain the regulatory mechanism underlying LPS-mediated necroptosis. Altogether, our results demonstrated that septic cardiomyopathy is associated with an activation of necroptosis through the Ripk3/Pgam5 signaling pathway.
细胞坏死是一种新型的细胞死亡方式。然而，细胞坏死在 LPS 相关心肌细胞损伤中的作用尚未完全阐明。本研究旨在探讨炎症介导的心肌细胞坏死的分子机制。采用 LPS 处理 H9C2 心肌细胞系，通过 qPCR 和 ELISA 检测细胞活力和坏死程度。通过通路分析验证 Ripk3/Pgam5 信号通路是否参与调节心肌细胞坏死。结果表明，LPS 降低了心肌细胞活力并激活了坏死。在分子水平上，LPS 触发了氧化应激和炎症，这些改变可能导致坏死的激活。最后，我们发现 LPS 在心肌细胞中激活了 Ripk3/Pgam5 信号通路，该信号通路可能解释了 LPS 介导的坏死的调节机制。总之，我们的结果表明，脓毒症性心肌病与 Ripk3/Pgam5 信号通路的激活有关，通过该信号通路可诱导细胞坏死。
