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阴道刺激通过改变心脏居民巨细胞功能来拯救HFpEF

Thamizhiniyan Venkatesan¹, Maria Toumpourleka¹, Monika Niewiadomska¹

¹Cardiovascular Section, Department of Medicine (T.V., M.T., M.N., K.F., L.M., K.E., S.W., S.S.), University of Oklahoma Health Science Center.

Circulation research

|July 15, 2025

概括

通过皮肤的迷走神经刺激 (tVNS) 通过调节心脏巨细胞来改善心力衰竭与保存的喷射分数 (HFpEF). 这种神经免疫疗法减少了亲纤维细胞巨细胞并增强了修复性巨细胞,为HFpEF提供了一种新的治疗策略.

科学领域:

心血管研究研究心血管研究
免疫学免疫学免疫学
神经科学是一个神经科学.

背景情况:

通过皮肤的迷走神经刺激 (tVNS) 已经减少心脏纤维化和炎症在心力衰竭的老鼠模型与保存的喷射小部分 (HFpEF).
在HFpEF中,tVNS对心脏功能的有益影响背后的精确的巨介导机制尚不清楚.

研究的目的:

调查心脏居民巨细胞在HFpEF中的作用.
在HFpEF的小鼠模型中阐明tVNS改善心脏功能的机制.

主要方法:

在使用高脂肪饮食和L-NG-nitro arginine甲基的小鼠中诱导了保留喷射分数 (HFpEF) 的心力衰竭.
小鼠接受了穿皮漫神经刺激 (tVNS) 或假刺激,随后进行心脏功能分析 (心声图) 和免疫细胞分析 (单细胞RNA测序,流细胞计).
用基因操纵 (Spp1删除,Igf1删除) 和药理抑制 (α7nAChR) 来剖析信号通路.

主要成果:

HFpEF小鼠表现出腹功能障碍,左心室缩和纤维化,这些都是tVNS显著改善的.
HFpEF的特征是SPP1-表达CCR2+的心脏居民巨细胞 (CRM) 的积累.
tVNS降低了CCR2+CRM和SPP1的表达,同时增加了TLF+/MHC2+CRM中的IGF1表达. 删除SPP1或阻止CCR2+CRM改善了HFpEF,而在TLF+/MHC2+CRM中删除Igf1则扭转了tVNS的好处. 胆固醇信号干扰取消了tVNS的有效性.

结论:

通过皮肤的迷走神经刺激 (tVNS) 通过降低SPP1表达的CCR2+CRM和增加TLF+/MHC2+CRM中的亲修复性IGF1来改善HFpEF.
这些有益的效果通过胆固醇信号传递进行介导,为HFpEF治疗建立了一个新的神经免疫途径.
这些发现突出了tVNS作为一个有前途的治疗策略,针对HFpEF中的巨细胞极化.

关键词:

乙烯基胆是一种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?迷走神经刺激迷走神经刺激

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