Department of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Department of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan; Department of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka, Japan; Institute for Advanced Co-Creation Studies, Osaka University, Suita, Osaka, Japan.
Kidney Int. 2022 Jan;101(1):13-15. doi: 10.1016/j.kint.2021.10.021.
Acute kidney injury (AKI) increases the risk of chronic kidney disease (CKD), but the mechanisms of CKD development after AKI remain unclear. Recent studies have elucidated that autophagy protects against AKI, but the role of autophagy during the AKI-to-CKD transition is controversial. Beclin1 is a key molecule for autophagy as well as endocytosis and phagocytosis. Shi et al. demonstrate that Beclin1 activates autophagy and is a promising therapeutic target for AKI-to-CKD transition.
急性肾损伤 (AKI) 会增加慢性肾脏病 (CKD) 的风险，但 AKI 后 CKD 发展的机制仍不清楚。最近的研究表明自噬可预防 AKI，但自噬在 AKI 向 CKD 转变过程中的作用存在争议。Beclin1 是自噬以及内吞作用和吞噬作用的关键分子。Shi 等人证明 Beclin1 激活自噬，是 AKI 向 CKD 转变的有希望的治疗靶点。
