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巨衍生CCL24通过纤维细胞CCR3促进心脏纤维化

Preethy Parthiban¹, Fanta Barrow¹, Haiguang Wang¹

¹Department of Integrative Biology and Physiology (P.P., F.B., H.W., H.N., M.D., J.P.P., D.Y., E.C., A. Hakeem, X.S.R.), University of Minnesota, Minneapolis.

Circulation research

|September 16, 2025

概括

心脏寄居的巨细胞释放CCL24,一种化学激素,通过通过CCR3.3激活纤维细胞,使心力衰竭恶化. 阻止这种途径可以改善心脏功能,突出显示心力衰竭的潜在治疗点.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

炎症是心血管疾病发展和进展的关键因素.
巨细胞,特别是心脏居民巨细胞 (CRMs),在心脏重塑过程中至关重要.
CRMs影响心力衰竭重塑的确切机制尚未完全理解.

研究的目的:

为了研究心脏住宿巨细胞 (CRMs) 在心力衰竭中的作用.
确定CRMS调节心脏重塑的特定分子和途径.
探索针对心力衰竭中CRM衍生因素的治疗潜力.

主要方法:

在体内和体外模型中使用,包括小鼠的压力过载 (横向大动脉收缩).
使用CRISPR/Cas9技术生成了CCL24缺乏和纤维细胞特异性CCR3缺乏的小鼠.
研究了CCL24对心脏纤维细胞和下游信号通路 (PI3K,TGF-β) 的直接影响.

主要成果:

在压力过载时表达高水平的CCL24的CRM亚群被确定.
CCL24缺乏改善了心脏纤维化和心脏功能受伤后的改善.
CCL24通过CCR3直接激活心脏纤维细胞,通过PI3K和TGF-β促进增殖和纤维化.
纤维细胞特异性CCR3删除或CCL24-CCR3轴的药理阻塞改善了压力过载小鼠的心脏功能.

结论:

巨衍生的CCL24会加剧心脏纤维化,并通过CCR3受体损害心脏衰竭中的心脏功能.
CCL24-CCR3信号轴是缓解心力衰竭中不良心脏重塑的有希望的治疗标.

关键词:

纤维化纤维化心脏衰竭是因为心脏衰竭.这是一种炎症炎症炎症炎症.巨细胞是什么?巨细胞是什么?

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