UCH-L1 Expressed by Podocytes: a Potentially Therapeutic Target for Lupus Nephritis?

Overview

Journal Inflammation

Specialties Allergy & Immunology
Pathology

Date 2017 Jan 25

PMID 28116572

Citations 3

Authors

Ji-Hong Cui

Xin Xie

Affiliations

Soon will be listed here.

Abstract

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.

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