在失重环境暴露时,血管可发生结构与功能重塑，对航天员在轨和返回后的身体健康与工作能力将造成不利影响，相关机制仍未完全阐明。1-磷酸鞘胺醇（sphingosin-1-phosphate, S1P）是重要的鞘磷脂分子之一，与血管内皮、平滑肌、外膜细胞的生理调控和病理改变密切相关。自噬是维持血管正常状态的重要细胞过程，是S1P的关键下游机制。我们的前期研究发现模拟失重可致大鼠血管S1P和自噬发生改变并参与调节血管氧化应激及功能变化。因此推测：S1P/S1P受体（S1PRs）通过调控自噬在模拟失重大鼠血管结构与功能重塑中发挥重要作用。本工作将在整体动物、离体血管和培养细胞水平，继续深入阐明模拟失重对S1P/S1PRs的影响，探讨其在不同血管自噬调控、结构及功能变化、氧化应激和炎性反应改变中的作用和机制。所得结论将为航天飞行后的血管调控理论提供新的实验依据，亦可为完善载人航天医务保障提出新的思路。

Exposure to weightlessness induces vascular remodeling on structure and function imposing adverse influence on the health and working ability of spacemen both in orbit and back to the earth. The mechanisms are still to be elucidated. Sphingosin-1-phosphate (S1P) is one of the most important sphingolipids closely related to the physiological and pathophysiological regulation of endothelial cell, smooth muscle cell and adventitial cell of vascular system. Autophagy acts as the crucial cellular process to keep vascular structure and function proper of which S1P is a pivotal modulator. Our preliminary data showed the simulated weightlessness changed S1P/S1P receptor (S1PRs) significantly regulating autophagy which was involved in the structural and functional remodeling of artery. So we hypothesize that S1P/S1PRs mediates the vascular structural and functional adaptation to weightlessness by modifying autophagy. We would investigate the role of S1P/S1PRs controlled autophagy in remodeling of vascular system more deeply in vivo, in vitro and in cultured cells. Our conclusion might provide new evidence for the vascular healthy interference during space fly and also be helpful to raise new idea for the space medical protection. Given the development of manned space mission of our country and roadmap of long duration space fly, our project is to some extent theoretically and practically significant.