Immunity：李玉琳/李平/林灼锋团队利用光遗传学迷走神经刺激，减轻心力衰竭

Core Viewpoint - The study indicates that optogenetic vagal nerve stimulation (VNS) can alleviate heart failure (HF) by limiting the generation of monocyte-derived inflammatory CCRL2+ macrophages [2][3][4]. Summary by Sections Mechanism of Action - The research demonstrates that VNS reduces the proportion of CCRL2+ macrophages, which are derived from myeloid monocytes and exhibit unique tumor necrosis factor alpha (TNF-α) cytokine responses, hypertrophic, and fibrotic characteristics [4]. - The elimination of CCRL2+ macrophages can prevent cardiac remodeling and heart failure [4]. Key Findings - The study confirms a positive correlation between CCRL2+ macrophages and TNF-α responsive proteins in the human heart with cardiac remodeling and dysfunction [5]. - Activation of the α7 nicotinic acetylcholine receptor (α7nAChR) plays a crucial role in the cardiac protective effects mediated by VNS, as it inhibits the response of CCRL2+ macrophages to TNF-α by increasing the expression of the transcription factor NRF2 [4][5]. Therapeutic Implications - Overall, the results suggest that the vagus nerve-immune axis can regulate heart failure and represents a promising therapeutic target [6].