Progress of small ubiquitin-related modifiers in kidney diseases.
10.1097/CM9.0000000000000094
- Author:
Ou LI
1
;
Qian MA
;
Fei LI
;
Guang-Yan CAI
;
Xiang-Mei CHEN
;
Quan HONG
Author Information
1. Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases, Beijing 100853, China.
- Publication Type:Journal Article
- MeSH:
Acute Kidney Injury;
etiology;
Carcinoma, Renal Cell;
etiology;
Diabetic Nephropathies;
etiology;
Fibrosis;
Humans;
Kidney;
pathology;
Kidney Diseases;
etiology;
metabolism;
Kidney Neoplasms;
etiology;
SUMO-1 Protein;
physiology;
Sumoylation
- From:
Chinese Medical Journal
2019;132(4):466-473
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:Small ubiquitin-related modifiers (SUMOs) are a group of post-translational modification proteins extensively expressed in eukaryotes. Abnormal SUMOylation can lead to the development of various diseases. This article summarizes the progress on research of the role of SUMOs in various types of kidney diseases to further increase the understanding of the regulatory functions of SUMOylation in the pathogenesis of kidney diseases.
DATA SOURCES:This review was based on articles published in the PubMed databases up to January 2018, using the keywords including "SUMOs," "SUMOylation," and "kidney diseases."
STUDY SELECTION:Original articles and critical reviews about SUMOs and kidney disease were selected for this review. A total of 50 studies were in English.
RESULTS:SUMO participates in the activation of NF-κB inflammatory signaling pathway, playing a central regulatory role in the inflammation and progression of DN, and the secretion of various chemokines in AKI. SUMO involves in the regulation of TG2 and Nrf2 antioxidant stress, affecting renal tubular injury in AKI. SUMO affects the MAPK/ERK pathway, regulating intracellular signal transduction, modulating the transcription and expression of effector molecules in DN. SUMO contributes to the TGF-β/Smad pathway, leading to fibrosis of the kidney. The conjugate combination of SUMO and p53 regulates cell proliferation and apoptosis, and participates in the regulation of tumorigenesis. In addition, SUMOylation of MITF modulates renal tumors secondary to melanoma, Similarly, SUMOylation of tumor suppressor gene VHL regulates the occurrence of renal cell carcinoma in VHL syndrome.
CONCLUSIONS:Tissue injury, inflammatory responses, fibrosis, apoptosis, and tumor proliferation in kidney diseases all involve SUMOs. Further research of the substrate SUMOylation and regulatory mechanisms of SUMO in kidney diseases will improve and develop new treatment measures and strategies targeting kidney diseases.
