血管胶原重构是高血压发生、发展的重要病理基础，但其形成机制迄今为止尚不清楚。本课题组最近发现内源性二氧化硫可抑制高血压形成，在上述研究基础上本项目拟以自发性高血压大鼠为研究模型，观察高血压血管胶原重构形成中内源性二氧化硫体系的动态变化；采用基因操作干预或给予二氧化硫供体及内源性二氧化硫生成抑制剂，抑制或激活内源性二氧化硫生成，从整体和细胞水平研究二氧化硫对高血压血管胶原重构的调节作用；从胶原合成和胶原降解的动态平衡角度，研究二氧化硫调节高血压血管胶原重构的作用环节；以胶原代谢关键通路转化生长因子-beta（TGF-beta）/Smad信号为切入点，揭示二氧化硫调节高血压血管胶原重构的信号通路。通过上述研究，以期阐明内源性二氧化硫对高血压血管胶原重构的调节作用、作用环节及信号通路，从胶原代谢失衡角度进一步深化高血压血管重构的发生机制。

Vascular collagen remodeling is one of important pathology in the formation and development of hypertension. But so far, its pathogenesis has been unclear. Our research group recently found that endogenous sulfur dioxide could inhibit the development of hypertension. Based on the above studies, the present study is designed to analyze the change of endogenous sulfur dioxide pathway in abnormal deposition of vascular collagen in hypertensive rats and investigate the regulatory effect of sulfur dioxide on abnormal synthesis and degradation of vascular collagen by using gene manipulation or sulfur dioxide donor or endogenous sulfur dioxide production inhibitor in vivo and in vitro. Targeting to TGF-beta/Smad signaling pathway, a key pathway of collagen metabolism, the study aims to explore the molecular mechanisms by which sulfur dioxide regulates excessive accumulation of vascular collagen in hypertension. The study would further disclose the regulatory effect of endogenous sulfur dioxide on hypertensive vascular collagen remodeling and its mechanisms, providing the new research direction for the pathogenesis of hypertension.