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Deciphering the SUMO code in the kidney
Author(s) -
Yang Zhen,
Zhang Yuming,
Sun Shiren
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14021
Subject(s) - kidney , podocyte , pathogenesis , fibrosis , medicine , bioinformatics , cancer research , kidney disease , biology , pathology , immunology , proteinuria
SUMO ylation of proteins is an important regulatory element in modulating protein function and has been implicated in the pathogenesis of numerous human diseases such as cancers, neurodegenerative diseases, brain injuries, diabetes, and familial dilated cardiomyopathy. Growing evidence has pointed to a significant role of SUMO in kidney diseases such as DN , RCC , nephritis, AKI , hypertonic stress and nephrolithiasis. Recently, emerging studies in podocytes demonstrated that SUMO might have a protective role against podocyte apoptosis. However, the SUMO code responsible for beneficial outcome in the kidney remains to be decrypted. Our recent experiments have revealed that the expression of both SUMO and SUMO ylated proteins is appreciably elevated in hypoxia‐induced tubular epithelial cells ( TEC s) as well as in the unilateral ureteric obstruction ( UUO ) mouse model, suggesting a role of SUMO in TEC s injury and renal fibrosis. In this review, we attempt to decipher the SUMO code in the development of kidney diseases by summarizing the defined function of SUMO and looking forward to the potential role of SUMO in kidney diseases, especially in the pathology of renal fibrosis and CKD , with the goal of developing strategies that maximize correct interpretation in clinical therapy and prognosis.

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