Department of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Department of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Int Immunopharmacol. 2024 Sep 30;139:112664. doi: 10.1016/j.intimp.2024.112664. Epub 2024 Jul 14.
PANoptosis is a newly discovered type of cell death characterized by pyroptosis, apoptosis and/or necroptosis and has been implicated in the inflammatory response. Piezo1 is a mechanosensitive ion channel that plays important roles in physiological development and various diseases. However, whether cardiomyocytes undergo PANoptosis during myocardial ischaemia/reperfusion (I/R) injury and the role of Piezo1 in this process remain largely unexplored. In this study, our results revealed that the expression levels of the main components of the PANoptosome, including caspase-8, caspase-3, NLRP3, caspase-1, GSDMD, RIPK1, RIPK3 and MLKL, were significantly upregulated in I/R heart tissues over time, indicating the occurrence of PANoptosis in I/R hearts. Accordingly, Piezo1 expression was significantly upregulated in I/R-injured hearts and hypoxia/reoxygenation (H/R)-treated cardiomyocytes. In contrast, pharmacological inhibition of Piezo1 by the inhibitor GsMTx4 in mice markedly attenuated the I/R-mediated decline in cardiac contractile function and increases in infarct size, apoptosis, oxidative stress and inflammation accompanied by the inhibition of PANoptosis-related mediators in I/R hearts. Consistently, the effects of Piezo1 on calcium influx and PANoptosis were further verified by GsMTx4 and Piezo1 activator Yoda1 in H/R-treated cardiomyocytes in vitro. Moreover, caspase-8 rather than calcium influx was required for H/R-induced PANoptosis in vitro. Mechanistically, Piezo1 interacts with caspase-8, a key initial activator of the PANoptosome complex, which subsequently activates cardiomyocyte PANoptosis, leading to cardiac dysfunction. In summary, these data suggest that Piezo1 is a new cardiac mechanosensor that promotes cardiac I/R injury possibly through the caspase-8-mediated activation of cardiomyocyte PANoptosis and highlight that Piezo1 may represent a new target for treating ischaemic heart disease.
细胞焦亡性细胞程序性坏死是一种新发现的细胞死亡方式,其特征为细胞焦亡、细胞凋亡和/或细胞坏死,并与炎症反应有关。Piezo1 是一种机械敏感性离子通道,在生理发育和各种疾病中发挥重要作用。然而,心肌缺血/再灌注(I/R)损伤过程中心肌细胞是否发生细胞焦亡性细胞程序性坏死以及 Piezo1 在该过程中的作用在很大程度上仍未得到探索。在本研究中,我们的结果表明,随着时间的推移,I/R 心脏组织中 PANoptosome 的主要成分,包括 caspase-8、caspase-3、NLRP3、caspase-1、GSDMD、RIPK1、RIPK3 和 MLKL 的表达水平显著上调,表明 I/R 心脏中发生了细胞焦亡性细胞程序性坏死。相应地,Piezo1 在 I/R 损伤的心脏和缺氧/复氧(H/R)处理的心肌细胞中表达显著上调。相反,用 Piezo1 抑制剂 GsMTx4 对小鼠进行药理学抑制可显著减轻 I/R 介导的心脏收缩功能下降和梗死面积增加、凋亡、氧化应激和炎症,并抑制 I/R 心脏中与 PANoptosis 相关的介质。同样,用 GsMTx4 和 Piezo1 激活剂 Yoda1 在体外 H/R 处理的心肌细胞中进一步验证了 Piezo1 对钙内流和 PANoptosis 的影响。此外,在体外,caspase-8 而不是钙内流是 H/R 诱导的 PANoptosis 所必需的。在机制上,Piezo1 与 caspase-8 相互作用,caspase-8 是 PANoptosome 复合物的关键初始激活剂,随后激活心肌细胞的 PANoptosis,导致心脏功能障碍。综上所述,这些数据表明 Piezo1 是一种新的心脏机械感受器,可能通过 caspase-8 介导的心肌细胞 PANoptosis 激活促进心脏 I/R 损伤,并强调 Piezo1 可能成为治疗缺血性心脏病的新靶点。