糖尿病肾病（DN）作为终末期肾病的主要原因，足细胞损伤是其发展的关键因素，而足细胞的损伤和线粒体自噬密切相关。我们认为糖尿病肾病的中医核心病机是“热邪致癥”，在此理论指导下的清热消癥法可以调控自噬延缓糖尿病肾病进展。基于调控线粒体自噬可能延缓DN的基础上，我们提出“清热消癥法可以通过激活线粒体自噬，保护线粒体功能，减轻肾脏足细胞的损伤和凋亡，从而延缓DN进展”的假说。本研究以高糖刺激的肾脏足细胞模型以及沉默ULK1的足细胞模型为研究对象，探讨清热消癥方是否可以通过调控ULK1的表达，干预AMPK-ULK1通路，激活线粒体自噬发挥保护线粒体作用，阐明清热消癥方治疗DN与激活线粒体自噬的相关性，验证假说的科学性与客观性，探讨清热消癥方治疗DN的确切作用靶点及效应机制，为以“肾络癥瘕”理论为指导的中医药防治糖尿病肾病研究提供中医理论基础和实验依据。

Diabetic nephropathy (DN) is the main cause of end-stage nephropathy, and podocyte injury is the key factor for its development, while the injury of podocyte is closely related to mitochondrial autophagy. We believe that the core pathogenesis of diabetic nephropathy in traditional Chinese medicine is "ReXieZhiZhen ". Under the guidance of this theory, the method of clearing away heat and eliminating symptoms can regulate autophagy and delay the progression of diabetic nephropathy. On the basis that regulating mitochondrial autophagy may delay DN, we proposed the hypothesis that “QingReXiaoZheng Fa” can delay DN progression by activating mitochondrial autophagy, protecting mitochondrial function, and alleviating renal podocyte injury and apoptosis". This research by the high sugar stimulating kidney podocytes model and knocking down ULK1 model as the research object, explore “QingReXiaoZheng Fa”whether can regulate the expression of ULK1, intervention AMPK - ULK1 pathways, activate the mitochondria play a role of protecting mitochondrial autophagy, clarify QingReXiaoZheng Fa treatment of DN and activate the correlation of mitochondrial autophagy, verify the hypothesis is scientific and objective, to explore the exact effect of heat dissipation disease party in the treatment of DN targets and effect mechanism, to "ShenLouZhengJia " theory as the instruction of TCM prevention and treatment of diabetic nephropathy research and provide the theoretical basis and experimental basis of traditional Chinese medicine.