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类似于resistin的γ分子攻击心肌细胞膜,并促进腹腔心动减速

Nina Kumowski^1,2,3, Steffen Pabel^1,2,3,4, Jana Grune^1,2

¹Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.)

|September 4, 2025

概括

中性粒细胞通过类似于阻力素的玛分子 (RELMγ) 促进心律失常,如心室低心率. 在小鼠中删除RELMγ减少了这些危险的心律障碍,揭示了突然心脏死亡的新机制.

科学领域:

心血管研究
免疫学
分子生物学

背景情况:

风性心律失常 (VT) 是与心肌梗塞相关的危及生命的心律失常.
中性粒细胞透到缺血性心脏并导致静脉瘤的发展.
中性粒细胞促进静脉瘤的特定分子机制尚不完全理解.

研究的目的:

研究心肌梗塞诱导静脉瘤期间中性粒细胞中差异表达基因的作用.
确定用于预防或治疗静脉瘤的新分子点.

主要方法:

在小鼠心脏病模型中对中性粒细胞和巨细胞的比较基因表达分析.
产生白细胞特异性的*Retnlg*灭绝小鼠.
在绝杀和野生类型小鼠中评估心电生理学和心肌细胞完整性.
使用脂质体和哺乳动物细胞进行体外研究,以评估抗体样分子玛 (RELMγ) 和人类抗体的膜破坏作用.

主要成果:

在心脏病发作区域内的中性粒细胞中,抵抗类分子马 (RELMγ) 显著上调.
在急性心肌梗塞的小鼠中,白细胞特异性删除*Retnlg*显著降低了静脉瘤的发生率.
在心肌细胞中诱导了RELMγ的膜透性,导致分极后延迟和随后的细胞死亡,这两者都是强大的心律失常触发剂.
人类抵抗素在脂质体和哺乳动物细胞上表现出类似的膜破坏活性.

结论:

形成孔隙的蛋白质RELMγ是心肌梗塞后中性粒细胞诱导静脉瘤的关键媒介.
这种机制直接损害心肌细胞膜,造成电动不稳定.
针对RELMγ是一种潜在的治疗策略,可以预防心律失常导致的突然心脏死亡.

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