Erratum to “Deletion of protein tyrosine phosphatase SHP-1 restores SUMOylation of podocin and reverses the progression of diabetic kidney disease.” Kidney Int. 2023;104:787–802

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DOI of original article: https://doi.org/10.1016/j.kint.2023.06.038 It was discovered that the XML version of the above article contained errors in the graphical abstract that were not the fault of the authors. The Publisher decided to “resupply” (repost and replace) the XML version of the article. Elsevier regrets and apologizes for any inconvenience caused by posting a new version of this article online but hopes that the reader will understand the reasons for doing so. Deletion of protein tyrosine phosphatase SHP-1 restores SUMOylation of podocin and reverses the progression of diabetic kidney diseaseKidney InternationalVol. 104Issue 4PreviewBoth clinical and experimental data suggest that podocyte injury is involved in the onset and progression of diabetic kidney disease (DKD). Although the mechanisms underlying the development of podocyte loss are not completely understood, critical structural proteins such as podocin play a major role in podocyte survival and function. We have reported that the protein tyrosine phosphatase SHP-1 expression increased in podocytes of diabetic mice and glomeruli of patients with diabetes. However, the in vivo contribution of SHP-1 in podocytes is unknown. Full-Text PDF Open Access

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