有氧运动抑制gsdme依赖性心肌细胞焦亡保护缺血再灌注损伤。

IF 6 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular Medicine Pub Date : 2024-12-24 DOI:10.1186/s10020-024-01048-7

Yi Li, Xiang Wang, Xuyang Meng, Chenxi Xia, Chenguang Yang, Jun Wang, Jiefu Yang, Fang Wang

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引用次数: 0

摘要

背景：急性心肌梗死（AMI）仍然是全球死亡的一个重要原因，缺血再灌注（IR）损伤加剧了急性心肌梗死。心肌细胞焦亡是影响IR损伤严重程度的重要途径。方法：通过观察IGFBP2的调节及其对gsdme依赖性心肌细胞焦亡的影响，探讨有氧运动对IR损伤的心脏保护作用。利用免疫印迹分析、ELISA、免疫荧光和超声心动图探索其机制途径。结果：我们的研究结果表明，有氧运动可以增加IGFBP2的循环水平，从而有效地抑制gsdme依赖性心肌细胞焦亡。这种调节通过AKT-GSK3β信号通路发生，涉及VDAC1磷酸化，从而增强线粒体功能并减少氧化应激。结论：总之，我们的研究强调了IGFBP2在减轻gsdme依赖性焦亡中的作用，这是有氧运动对IR损伤发挥心脏保护作用的一种机制。这些见解提示了治疗急性心肌梗死的潜在治疗靶点。

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Aerobic exercise inhibits GSDME-dependent myocardial cell pyroptosis to protect ischemia-reperfusion injury.

Background: Acute myocardial infarction (AMI) remains a significant cause of global mortality, exacerbated by ischemia-reperfusion (IR) injury. Myocardial cell pyroptosis has emerged as a critical pathway influencing IR injury severity.

Methods: We aimed to investigate the cardioprotective effects of aerobic exercise on IR injury by examining the modulation of IGFBP2 and its impact on GSDME-dependent myocardial cell pyroptosis. Mechanistic pathways were explored using western blot analysis, ELISA, immunofluorescence, and echocardiography.

Results: Our findings demonstrate that aerobic exercise leads to increased circulating levels of IGFBP2, which effectively suppresses GSDME-dependent myocardial cell pyroptosis. This regulation occurs via the AKT-GSK3β signaling pathway, involving VDAC1 phosphorylation, thereby enhancing mitochondrial function and reducing oxidative stress.

Conclusion: In conclusion, our study highlights the role of IGFBP2 in mitigating GSDME-dependent pyroptosis as a mechanism through which aerobic exercise exerts cardioprotective effects against IR injury. These insights suggest potential therapeutic targets for managing acute myocardial infarction.

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来源期刊

Molecular Medicine 医学-生化与分子生物学

CiteScore

8.60

自引率

0.00%

发文量

137

审稿时长

1 months

期刊介绍： Molecular Medicine is an open access journal that focuses on publishing recent findings related to disease pathogenesis at the molecular or physiological level. These insights can potentially contribute to the development of specific tools for disease diagnosis, treatment, or prevention. The journal considers manuscripts that present material pertinent to the genetic, molecular, or cellular underpinnings of critical physiological or disease processes. Submissions to Molecular Medicine are expected to elucidate the broader implications of the research findings for human disease and medicine in a manner that is accessible to a wide audience.