抵抗素样分子γ攻击心肌细胞膜，促进室性心动过速，这一成果由
将中性粒细胞与巨噬细胞进行比较，研究团队发现抵抗素样分子γ （Retnlg或RELMγ）是单核细胞梗死中差异表达最多的基因。RELMγ是一个成孔蛋白家族的一部分，它通过穿孔细菌的膜来保护宿主免受细菌的侵害。在急性梗死小鼠中，白细胞特异性retlg缺失可降低室性心动过速。RELMγ引发膜缺陷，允许细胞排斥染料进入心肌细胞内部，也导致延迟的去极化和后来的心肌细胞死亡，这两者都是强烈的心律失常触发因素。人类抵抗素同样攻击脂质体和哺乳动物细胞的膜。课题组人员描述了如何误导先天免疫防御产生膜泄漏和室性心律失常。
据悉，室性心动过速破坏心脏的协调泵功能，导致心源性猝死。大量的中性粒细胞聚集到缺血心肌中，促进了这些心律失常。
附：英文原文
Title: Resistin-like molecule γ attacks cardiomyocyte membranes and promotes ventricular tachycardia
Author: Nina Kumowski, Steffen Pabel, Jana Grune, Noor Momin, Van K. Ninh, Laura Stengel, Kyle I. Mentkowski, Yoshiko Iwamoto, Yi Zheng, I-Hsiu Lee, Jessica Matthias, Jan O. Wirth, Fadi E. Pulous, Hana Seung, Alexandre Paccalet, Charlotte G. Muse, Kenneth K. Y. Ting, Paul Delgado, Andrew J. M. Lewis, Vaishali Kaushal, Antonia Kreso, Dennis Brown, Sikander Hayat, Rafael Kramann, Filip K. Swirski, Kamila Naxerova, Daniel C. Propheter, Lora V. Hooper, Michael A. Moskowitz, Kevin R. King, Nadia Rosenthal, Maarten Hulsmans, Matthias Nahrendorf
Issue&Volume: 2025-09-04
Abstract: Ventricular tachycardia disrupts the heart’s coordinated pump function, leading to sudden cardiac death. Neutrophils, which are recruited in high numbers to the ischemic myocardium, promote these arrhythmias. Comparing neutrophils with macrophages, we found that resistin-like molecule γ (Retnlg or RELMγ) was the most differentially expressed gene in mouse infarcts. RELMγ is part of a pore-forming protein family that defends the host against bacteria by perforating their membranes. In mice with acute infarcts, leukocyte-specific Retnlg deletion reduced ventricular tachycardia. RELMγ elicited membrane defects that allowed cell exclusion dyes to enter the cardiomyocyte interior and also caused delayed afterdepolarizations and later cardiomyocyte death, both of which are strong arrhythmogenic triggers. Human resistin likewise attacked membranes of liposomes and mammalian cells. We describe how misdirected innate immune defense produces membrane leaks and ventricular arrhythmia.
DOI: adp7361
Source: https://www.science.org/doi/10.1126/science.adp7361