《生命科学》 2026, 38(7): 1221-1230
运动重编程母体肥胖子代血管功能障碍的研究进展
摘 要：
肥胖已成为全球公共卫生挑战，其在育龄期女性中的发生率持续上升。母体肥胖不仅危害孕妇自身健康， 还可通过发育源性机制对子代心血管系统产生深远影响，增加其成年后罹患心血管疾病的风险。血管功能障碍是 母体肥胖对子代心血管系统产生不良影响的关键环节，表现为内皮功能受损、血管结构重塑及血管反应性异常。作 为一种安全有效的非药物干预手段，母体规律运动可对子代血管系统实现重编程，通过优化宫内环境、改善胎盘结 构与功能及调节表观遗传修饰，缓解母体肥胖的不良代际效应。本综述旨在总结母体肥胖对子代血管的不良编程 效应，探讨运动的重编程效果及潜在的分子机制，为探索通过有效运动干预阻断肥胖代际传递提供理论参考。
通讯作者：张严焱 , Email:yanyanzhang@bsu.edu.cn
Abstract:
Obesity has become a major global public health challenge, with a rapidly increasing incidence among women of reproductive age. Growing evidence indicates that maternal obesity not only impairs maternal metabolic health but also predisposes offspring to long-term cardiovascular diseases through developmental programming mechanisms. According to the developmental origins of health and disease (DOHaD) hypothesis, exposure to an obesogenic intrauterine environment confers persistent cardiovascular vulnerability across the lifespan. Vascular dysfunction is a key early manifestation linking maternal obesity to offspring cardiovascular risk. Offspring exposed to maternal obesity commonly exhibit vascular structural remodeling, including increased arterial stiffness and altered vascular wall composition, together with abnormal vascular reactivity and blood pressure regulation. Endothelial dysfunction is also frequently observed, characterized by impaired endothelium-dependent vasodilation, reduced nitric oxide bioavailability, and increased oxidative stress. These vascular abnormalities may arise early in life and persist into adulthood, contributing to the development of hypertension and cardiometabolic disorders. Exercise has emerged as a safe and effective non- pharmacological strategy to counteract obesity-induced adverse vascular programming. Evidence from both human and animal studies suggests that maternal exercise before and during pregnancy improves offspring vascular structure and function, while postnatal exercise may further ameliorate vascular dysfunction during childhood and adolescence. The magnitude of these benefits appears to depend on the timing and characteristics of the exercise intervention, with the prenatal period representing a particularly sensitive window. Mechanistically, exercise-induced vascular reprogramming involves multiple interrelated pathways. Maternal exercise improves the intrauterine environment by attenuating inflammation and oxidative stress, thereby preserving endothelial nitric oxide signaling and redox balance in offspring. In parallel, exercise promotes beneficial placental adaptations, including enhanced placental vascularization, improved mitochondrial function, and optimized nutrient and oxygen transport, supporting normal fetal vascular development. In addition, accumulating evidence highlights epigenetic regulation as a central mechanism underlying long-term vascular reprogramming. Exercise modulates DNA methylation, histone modifications, and non-coding RNA expression in offspring vascular tissues, leading to persistent alterations in genes involved in vascular tone regulation, oxidative stress responses, and endothelial function. Further studies are needed to elucidate the optimal exercise strategies and the mechanisms underlying long-term vascular reprogramming, thereby facilitating the prevention of cardiovascular disease across generations.
Communication Author：ZHANG Yan-Yan , Email:yanyanzhang@bsu.edu.cn
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