Elia Andrea, Fossati Silvia
Department of Neural Sciences, Alzheimer's Center at Temple (ACT), Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Front Physiol. 2023 Jan 30;14:1060666. doi: 10.3389/fphys.2023.1060666. eCollection 2023.
The heart is a functional syncytium controlled by a delicate and sophisticated balance ensured by the tight coordination of its several cell subpopulations. Accordingly, cardiomyocytes together with the surrounding microenvironment participate in the heart tissue homeostasis. In the right atrium, the sinoatrial nodal cells regulate the cardiac impulse propagation through cardiomyocytes, thus ensuring the maintenance of the electric network in the heart tissue. Notably, the central nervous system (CNS) modulates the cardiac rhythm through the two limbs of the autonomic nervous system (ANS): the parasympathetic and sympathetic compartments. The autonomic nervous system exerts non-voluntary effects on different peripheral organs. The main neuromodulator of the Sympathetic Nervous System (SNS) is norepinephrine, while the principal neurotransmitter of the Parasympathetic Nervous System (PNS) is acetylcholine. Through these two main neurohormones, the ANS can gradually regulate cardiac, vascular, visceral, and glandular functions by turning on one of its two branches (adrenergic and/or cholinergic), which exert opposite effects on targeted organs. Besides these neuromodulators, the cardiac nervous system is ruled by specific neuropeptides (neurotrophic factors) that help to preserve innervation homeostasis through the myocardial layers (from epicardium to endocardium). Interestingly, the dysregulation of this neuro-signaling pathway may expose the cardiac tissue to severe disorders of different etiology and nature. Specifically, a maladaptive remodeling of the cardiac nervous system may culminate in a progressive loss of neurotrophins, thus leading to severe myocardial denervation, as observed in different cardiometabolic and neurodegenerative diseases (myocardial infarction, heart failure, Alzheimer's disease). This review analyzes the current knowledge on the pathophysiological processes involved in cardiac nervous system impairment from the perspectives of both cardiac disorders and a widely diffused and devastating neurodegenerative disorder, Alzheimer's disease, proposing a relationship between neurodegeneration, loss of neurotrophic factors, and cardiac nervous system impairment. This overview is conducive to a more comprehensive understanding of the process of cardiac neuro-signaling dysfunction, while bringing to light potential therapeutic scenarios to correct or delay the adverse cardiovascular remodeling, thus improving the cardiac prognosis and quality of life in patients with heart or neurodegenerative disorders.
心脏是一个功能性合胞体,由其多个细胞亚群紧密协调所确保的微妙而复杂的平衡控制。因此,心肌细胞与周围的微环境共同参与心脏组织的稳态。在右心房,窦房结细胞通过心肌细胞调节心脏冲动的传播,从而确保心脏组织中电网络的维持。值得注意的是,中枢神经系统(CNS)通过自主神经系统(ANS)的两个分支调节心律:副交感神经和交感神经部分。自主神经系统对不同的外周器官产生非自主作用。交感神经系统(SNS)的主要神经调节剂是去甲肾上腺素,而副交感神经系统(PNS)的主要神经递质是乙酰胆碱。通过这两种主要的神经激素,ANS可以通过开启其两个分支之一(肾上腺素能和/或胆碱能)来逐渐调节心脏、血管、内脏和腺体功能,这两个分支对目标器官产生相反的作用。除了这些神经调节剂外,心脏神经系统还受特定神经肽(神经营养因子)的调节,这些神经肽有助于通过心肌层(从心外膜到心内膜)维持神经支配稳态。有趣的是,这种神经信号通路的失调可能使心脏组织面临不同病因和性质的严重疾病。具体而言,心脏神经系统的适应性不良重塑可能最终导致神经营养因子的逐渐丧失,从而导致严重的心肌去神经支配,这在不同的心脏代谢和神经退行性疾病(心肌梗死、心力衰竭、阿尔茨海默病)中都有观察到。本综述从心脏疾病和广泛传播且具有破坏性的神经退行性疾病阿尔茨海默病的角度分析了目前关于心脏神经系统损伤所涉及的病理生理过程的知识,提出了神经退行性变、神经营养因子丧失和心脏神经系统损伤之间的关系。这一概述有助于更全面地理解心脏神经信号功能障碍的过程,同时揭示潜在的治疗方案,以纠正或延迟不良的心血管重塑,从而改善患有心脏或神经退行性疾病患者的心脏预后和生活质量。