Neuroimmune cross-talk in heart failure.

IF 10.2 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Sabrina Montuoro, Francesco Gentile, Alberto Giannoni
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引用次数: 0

Abstract

Heart failure (HF) is characterized by autonomic nervous system (ANS) imbalance and low-grade chronic inflammation. The bidirectional relationship between the ANS and immune system (IS) is named "neuroimmune cross-talk" (NICT), and is based on common signaling molecules, receptors, and pathways. NICT may be altered in HF, and neuroinflammation seems to be a main driver of HF progression. In HF, heightened sympathetic nerve activity triggers inflammatory cascades that lead to cardiomyocyte death and myocardial interstitial fibrosis. Concurrently, parasympathetic withdrawal may impair the cholinergic anti-inflammatory pathway, with a less effective immune response to infections or inflammatory events. Additionally, microglial activation and inflammatory molecules contribute to autonomic imbalance by acting on central nuclei and peripheral visceral feedbacks, which in turn promote adverse cardiac remodeling, HF decompensation, and potentially life-threatening arrhythmias. Therefore, neuroinflammation has been identified as a potential target for treatment. Pharmacological antagonism of the neurohormonal system remains the cornerstone of chronic HF therapy. While some drugs used in HF management may have additional benefits due to their anti-inflammatory properties, clinical trials targeting inflammation in patients with HF have so far produced inconclusive results. Nevertheless, considering the pathophysiological relevance of NICT, its modulation seems an appealing strategy to optimize HF management. Current research is therefore investigating novel pharmacological targets for anti-inflammatory drugs, and the immunomodulatory properties of denervation approaches and bioelectronic medicine devices targeting NICT and neuroinflammation in HF. A deeper understanding of the complex relationship between the ANS and IS, as outlined in this review, could therefore facilitate the design of future studies aimed at improving outcomes by targeting NICT in patients with HF.

心力衰竭中的神经免疫交叉对话
心力衰竭(HF)的特点是自律神经系统(ANS)失衡和低度慢性炎症。自律神经系统和免疫系统(IS)之间的双向关系被命名为 "神经免疫交叉对话"(NICT),其基础是共同的信号分子、受体和通路。在高血脂症中,NICT 可能会发生改变,而神经炎症似乎是高血脂症进展的主要驱动因素。在高房颤动中,交感神经活动增强会引发炎症级联反应,导致心肌细胞死亡和心肌间质纤维化。同时,副交感神经功能减退可能会损害胆碱能抗炎途径,从而降低对感染或炎症事件的免疫反应。此外,小胶质细胞活化和炎症分子通过作用于中枢神经核和外周内脏反馈,导致自律神经失衡,进而促进不良的心脏重塑、高房颤动失代偿和可能危及生命的心律失常。因此,神经炎症已被确定为潜在的治疗靶点。药物拮抗神经激素系统仍然是慢性高血压治疗的基石。虽然一些用于治疗高血压的药物可能因其抗炎特性而带来额外的益处,但针对高血压患者炎症的临床试验迄今为止尚未得出结论。尽管如此,考虑到 NICT 的病理生理学相关性,对其进行调节似乎是优化心房颤动治疗的一种有吸引力的策略。因此,目前的研究正在调查新型抗炎药物的药理靶点,以及针对高房颤动中的 NICT 和神经炎症的神经支配方法和生物电子医学设备的免疫调节特性。因此,深入了解自律神经系统与 IS 之间的复杂关系(如本综述所述)有助于设计未来的研究,从而通过针对高血压患者的 NICT 改善预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cardiovascular Research
Cardiovascular Research 医学-心血管系统
CiteScore
21.50
自引率
3.70%
发文量
547
审稿时长
1 months
期刊介绍: Cardiovascular Research Journal Overview: International journal of the European Society of Cardiology Focuses on basic and translational research in cardiology and cardiovascular biology Aims to enhance insight into cardiovascular disease mechanisms and innovation prospects Submission Criteria: Welcomes papers covering molecular, sub-cellular, cellular, organ, and organism levels Accepts clinical proof-of-concept and translational studies Manuscripts expected to provide significant contribution to cardiovascular biology and diseases
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