Key Laboratory of Resource Biology and Biotechnology in Western China (Northwest University), Ministry of Education, Xi'an, People's Republic of China.
College of Life Science, Northwest University, Xi'an, 710069, People's Republic of China.
Inflammation. 2017 Apr;40(2):657-665. doi: 10.1007/s10753-017-0512-x.
Systemic lupus erythematosus (SLE) is a multisystem disease affecting many organs, and the most severe complication is lupus nephritis. Podocyte injury and loss play vital roles in the pathogenesis of lupus nephritis. Studies have shown that ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) is involved in the pathogenesis and progression of many diseases, such as neurodegenerative disorders, cancers, and diabetes. Recently, numerous studies have indicated that UCH-L1 was upregulated in the podocytes in immune complex-mediated glomerulonephritis. This increase was correlated with disease aggravation. In this review, we discuss the role and mechanism of UCH-L1 in the pathogenesis of many diseases and, particularly, in lupus nephritis. Hence, we highlight the role of UCH-L1 in lupus nephritis.
系统性红斑狼疮（SLE）是一种多系统疾病，影响许多器官，最严重的并发症是狼疮性肾炎。足细胞损伤和丢失在狼疮性肾炎的发病机制中起着至关重要的作用。研究表明，泛素羧基末端水解酶 L1（UCH-L1）参与许多疾病的发病机制和进展，如神经退行性疾病、癌症和糖尿病。最近，许多研究表明，免疫复合物介导的肾小球肾炎中足细胞的 UCH-L1 上调，这种增加与疾病加重相关。在这篇综述中，我们讨论了 UCH-L1 在许多疾病发病机制中的作用和机制，特别是在狼疮性肾炎中的作用。因此，我们强调了 UCH-L1 在狼疮性肾炎中的作用。
