《生命科学》 2026, 38(6): 1004-1016
血管衰老的基础与临床研究进展
摘 要：
血管衰老不仅是心脑血管疾病的共同病理基础，更是驱动全身系统性衰老的“中枢”（Senohub）。本综述系统梳理了该领域的最新进展。在基础研究层面，确立了血管作为衰老启动者的核心地位，揭示了内皮与平滑肌细胞的表观遗传、代谢重编程及免疫-血管交互等层级调控机制，以及衰老细胞通过外泌体与分泌组介导的复杂通讯网络。临床评估正迈向多模态与智能化，以人工智能血管年龄、无创微血管成像及多组学“衰老时钟”为代表，实现了更早期、精准的量化评估。干预策略从传统风险控制演进至靶向核心机制：Senolytics疗法展现逆转潜力但需警惕长期安全性；SGLT2抑制剂、GLP-1受体激动剂和特拉唑嗪等“老药新用”证据确凿，但需关注老年肌少症等特定风险。这些进展共同推动血管衰老的防治向“主动管理健康衰老”的精准医学新模式转变。
通讯作者：张存泰 , Email:ctzhang0425@163.com
Abstract:
Vascular aging is a pivotal pathophysiological process underlying cardiovascular morbidity and is increasingly recognized as a ″central hub″ (Senohub) that initiates and drives systemic organismal aging. This review aims to synthesize recent breakthroughs in the molecular mechanisms, innovative assessment technologies, and emerging therapeutic interventions for vascular aging, providing a strategic roadmap for future translational research and clinical practice. At the basic research level, we establish the theoretical framework of the vasculature as a ″Senohub″ that broadcasts aging signals to distant organs via secreted senoproteins (e.g., GAS6). The review moves beyond traditional signaling pathways to detail a hierarchical regulatory network: upstream epigenetic drivers (e.g., METTL14-mediated RNA m6A modification), core metabolic executors (e.g., TRAP1-mediated histone lactylation), and downstream amplifiers involving complex immunovascular crosstalk. Specifically, we highlight how senescent vascular cells recruit and interact with T cells, polarized macrophages, and neutrophil extracellular traps (NETs) to sustain a pro-inflammatory microenvironment. In the clinical domain, assessment strategies are shifting from single hemodynamic metrics to AI-driven multi-modal profiling. We evaluate innovations such as artificial intelligence-derived vascular age (AI-VA), retinal aging clocks, and ultra-high-field MRI, which offer superior sensitivity for early detection. Regarding interventions, the field is evolving from managing downstream risk factors to targeting upstream aging biology. We critically evaluate the potential of Senolytics (e.g., Dasatinib+Quercetin) to reverse arterial stiffness, while emphasizing the need to address safety concerns such as off-target effects and tissue repair impairment. Furthermore, we discuss the anti-aging pleiotropy of SGLT2 inhibitors, GLP-1 receptor agonists and Terazosin, providing specific guidance on mitigating risks like drug-induced sarcopenia in elderly populations. The field is undergoing a paradigm shift from ″reactive disease treatment″ to ″proactive vascular health management″. Future directions should focus on integrating spatial multi-omics and AI to construct digital models for precise risk stratification. Ultimately, safely targeting the ″Senohub″ via immune-modulation or precision senotherapeutics represents a promising breakthrough for extending healthspan and combating age-related multimorbidity.
Communication Author：ZHANG Cun-Tai , Email:ctzhang0425@163.com
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