急性肾损伤是由各种原因引起的短时间内肾功能快速减退，新的治疗靶点对该类患者的生存及预后意义重大。CAMKIα是一种丝氨酸／苏氨酸蛋白激酶，我们前期研究发现，CAMKIα在肾缺血再灌注引起的急性肾损伤小鼠肾脏中表达增高并发生活化，而抑制CAMKIα表达后，肾脏组织损伤加重，线粒体提取物中PINK1/Parkin含量减少。另外，我们前期研究表明CAMKIα可以磷酸化PINK1及Parkin。故我们提出CAMKIα可以通过磷酸化PINK1/Parkin，促进线粒体自噬，从而在肾缺血再灌注引起的急性肾损伤中发挥保护作用。本项目拟使用小鼠肾缺血再灌注模型及肾小管上皮细胞HK-2细胞ATP去除-补充模型，以明确CAMKIα在急性肾损伤中的变化、对线粒体自噬的调控机制，以及对PINK1/Parkin的作用，为肾缺血再灌注引起的急性肾损伤提供新的治疗靶点。

Acute kidney injury (AKI) is characterized by a rapid decline in renal function caused by various causes , and new therapeutic targets are of great significance to the survival and prognosis of patients. CAMKIα is a serine / threonine protein kinase. Our previous work found that expression and activation of CAMKIα is up regulated in renal ischemia-reperfusion injury model of mice . After inhibiting the expression of CAMKIα, ischemic AKI is aggravated and the level of PINK1 / Parkin in the mitochondria is down regulated. In addition, our previous study showed that CAMKIα can phosphorylate PINK1 and Parkin. Therefore, we propose that CAMKIα can promote mitophagy by phosphorylating PINK1/Parkin, thereby playing a renal protection role in ischemia AKI. This project will use the renal ischemia-reperfusion model of mice and the ATP depletion-repletion (ATP D-R) model of HK-2 cell to elucidate the role of CAMKIα in acute kidney injury, and its regulatory impact on mitophagy and PINK1/Parkin, thus provides a new therapeutic target for acute kidney injury caused by renal ischemia-reperfusion injury.