近年来，急性肾损伤(AKI)引起的慢性肾脏病(CKD)的发病率逐渐上升，因而明确急性损伤-慢性化的病理生理机制具有重大科学研究价值和临床意义。研究表明：透明质酸（hyaluronan，HA）特别是低分子HA在急性损伤-慢性化过程中显著增多，而低分子HA有激活炎症反应的功能，因而可能在急性损伤-慢性化过程中扮演重要角色。结合本课题组的有关缺血再灌注小鼠模型肾脏淋巴管的发现以及现有文献报道，我们提出猜想：急性损伤-慢性化过程中淋巴管的新生不够充分，大量低分子HA不能被引流清除而聚集在肾脏损伤部位，促进炎症反应，进一步加速了急性损伤-慢性化的进展。本课题中，我们将基于肾脏淋巴管的全新视角，诠释肾脏新生淋巴管调节HA转运、清除参与急性损伤-慢性化的机制，探索诱导淋巴管新生进而延缓肾脏急性损伤-慢性化的可行性。

Recently, the incidence of chronic kidney diseases（CKD）caused by acute kidney disease (AKI) increased gradually. It is of great scientific value and clinical significance to clear the pathophysiologic mechanism of AKI to CKD. Studies have shown that: hyaluronan(HA) especially low molecular weight HA derived from mesenchymal cells increase significantly in a AKI to CKD animal model, additionally, low molecular weight HA is able to active inflammatory response, which may play an important role in the process of AKI to CKD. We found large amount of HA synthesis in kidneys of our ischemia reperfusion injury(IRI) animal model, accompanied by insufficient lymphangiogenesis and renal fibrosis. Combined with the existing literature, we conjectured that due to the insufficient lymphangiogenesis, a large number of low molecular weight HA can not be transported and thus promote inflammation locally, further accelerate the progress of AKI to CKD. In this study, we will confirm the above-mentioned suppose and explore a new therapy to promote lymphangiogenesis in order to improve HA transport and to relief the progress of AKI to CKD.