中文摘要：

力学因素调控血管生理性稳态和病理性重建的机制是力学生物学中应力-生长研究的重要内容，迄今尚未完全阐明。蛋白质组学这一高通量、系统性的新技术在血管力学生物学领域的应用，将生物力学、蛋白质组学、生物信息学与分子生物学相关研究理念和研究技术相结合，能够为心血管疾病发病机理研究和血管重建药物治疗靶向的寻找提供一个全新的力学生物学视角，也体现了学科交叉融合的创新特色和科学价值。近年来，上海交通大学力学生物学研究所遵循“力学生物学实验发现现象-生物信息学分析-生物学实验验证结论”开展了多学科相结合的系统性研究，建立了可能的血管细胞内机械应力信号传导网络。此外，基于力-血管蛋白质组学研究，揭示了60多种新的、可能参与了机械应力细胞内信号传导过程的信号分子，并深入探讨部分分子在应力调控血管细胞功能中的作用及分子机制。在研究所工作的基础上，综述了近年来力-血管蛋白质组学相关研究进展。力-血管蛋白质组学的研究工作有望为高血压、动脉粥样硬化等心血管疾病血管重建病理机制揭示、临床治疗潜在靶点寻找提供重要的力学生物学实验依据。

英文摘要：

The mechanobiological mechanism in vascular homeostasis and vascular remodeling is one of the most important areas in stress-growth research, which is still unclear. Proteomics analysis, which is a high-throughput and systemic technic, is recently combined with biomechanics, bioinformatics and traditional molecular biology, and applied to demonstrate the mechanism of vascular remodeling induced by different kinds of mechanical stresses. These multidisciplinary and integrated technologies give new insights into understanding the mechanobiological mechanism of vascular remodeling and provide novel potential targets of clinical therapy on cardiovascular diseases. During recent years, the Institute of Mechanobiology ＆ Medical Engineering of Shanghai Jiao Tong University has launched systematic researches with 3 steps： phenomenon exploration with mechanobiological experiments, bioinformatics analysis, and biological and experimental verifications, which established a potential mechanotransduction networks and more than 60 kinds of the novel mechanoresponsive molecules as well. Further researches were performed to demonstrate the role of these molecules in regulation of cellular functions under different kinds of mechanical stimuli. This paper reviews the recent progresses in vascular proteomics and the relative researches on mechanobiology. Researches based on mechanics-proteomics technics may contribute to the understanding of the pathogenesis of cardiovascular diseases, and provide novel therapeutic targets for vascular remodeling during hypertension and atherosclerosis.