神经血管界面的衰老：连接心血管与脑血管疾病的整合框架
Aging at the neurovascular interface: An integrative framework linking cardiovascular and cerebrovascular diseases.
摘要(中文译文)
衰老是心脑血管共病的基本驱动因素，然而衰老与心脑疾病并发之间的机制仍未被完全阐明。神经血管界面（NVI）是指神经、血管和细胞外基质信号相互作用的结构与功能界面。在中枢神经系统中，这一概念与经典神经血管单元在很大程度上重叠；而在心脏中，它指的是一个新兴的心脏组织特异性界面，涉及冠状动脉微血管、血管细胞、自主神经和感觉神经纤维、心肌细胞以及细胞外基质成分。尽管衰老通过NVI影响心脑血管共病的直接实验证据仍在积累中，但现有证据提示衰老可能破坏共有的神经血管特征。这些变化与高血压、脑小血管病、心力衰竭及相关疾病有关。此外，遗传变异可能作为神经血管衰老的易感性修饰因素——从调节血管张力的NOS3到影响自主神经平衡的ADRB1和COMT。这些变异与心脑血管疾病风险相关，并可能代表上游分子决定因素，遗传易感性与衰老相关应激源通过其汇聚，改变NVI完整性并促进心脑血管共病。本综述综合了关于NVI结构与功能基础的现有证据，讨论了衰老如何可能破坏其完整性，并评估了其作为整合性框架将衰老相关血管、神经、炎症和细胞外基质改变与心脑血管共病联系起来的潜在作用。我们还概述了可能保护界面功能的潜在整合策略，包括生活方式干预、衰老细胞清除药物和基因指导的精准医学。
Abstract
Aging is a fundamental driver of cardiovascular and cerebrovascular comorbidities, yet the mechanisms linking aging to concurrent heart and brain diseases remain incompletely understood. The neurovascular interface (NVI) refers to the structural and functional interface through which neural, vascular, and extracellular-matrix signals interact. In the CNS, this concept substantially overlaps with the classical neurovascular unit, whereas in the heart it refers to an emerging heart tissue-specific interface involving coronary microvessels, vascular cells, autonomic and sensory nerve fibers, cardiomyocytes, and extracellular-matrix components. Although direct experimental evidence that aging affects cardiovascular and cerebrovascular comorbidity through NVI is still accumulating, current evidence suggests that aging may disrupt shared neurovascular features. These changes are associated with hypertension, cerebral small vessel disease, heart failure, and related disorders. Moreover, genetic variants may act as susceptibility modifiers of neurovascular aging - from NOS3 regulating vascular tone to ADRB1 and COMT affecting autonomic balance. These variants are associated with cardiovascular and cerebrovascular disease risk and may represent upstream molecular determinants through which genetic susceptibility and aging-related stressors converge to alter NVI integrity and promote cardiovascular-cerebrovascular comorbidity. This review synthesizes current evidence on the structural and functional basis of the NVI, discusses how aging may disrupt its integrity, and evaluates its potential role as an integrative framework linking aging-related vascular, neural, inflammatory, and extracellular-matrix alterations to cardiovascular-cerebrovascular comorbidity. We also outline potential integrated strategies that may preserve interface function, including lifestyle interventions, senolytics, and gene-guided precision medicine.
如何引用
AMA
Kexin Chen, Jun Ma, Yong Peng. Aging at the neurovascular interface: An integrative framework linking cardiovascular and cerebrovascular diseases.. Ageing research reviews. 2026; doi:10.1016/j.arr.2026.103285.
APA
Kexin Chen, Jun Ma, Yong Peng (2026). Aging at the neurovascular interface: An integrative framework linking cardiovascular and cerebrovascular diseases.. Ageing research reviews. https://doi.org/10.1016/j.arr.2026.103285
GB/T 7714
Kexin Chen, Jun Ma, Yong Peng. Aging at the neurovascular interface: An integrative framework linking cardiovascular and cerebrovascular diseases.[J]. Ageing research reviews, 2026 doi:10.1016/j.arr.2026.103285.
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