Misc

Hypertension is a significant risk factor for microangiopathy and cardiovascular complications in diabetic patients. The efficacy of mineralocorticoid receptor (MR) antagonists in impeding the advancement of diabetic nephropathy, along with the reduction in active renin concentration observed in diabetic retinopathy, strongly implies the involvement of MR overactivation in diabetic complications. This review provides a comprehensive review of various mechanisms proposed for MR overactivation in diabetes mellitus. In particular, it focuses on post-translational MR modifications, including O-linked N-acetylglucosamine modification and phosphorylation, which have been implicated in MR protein stabilization and overactivation under conditions of high glucose. Given the role of MR overactivation in hyperglycemia, it emerges as a promising therapeutic target for preventing diabetic complications. Post-translational modifications (PTMs), such as O-GlcNAcylation and phosphorylation, are related to MR overactivation in diabetes and metabolic syndrome. Aldosterone binding promotes the proteasomal degradation of MR. Under conditions of high glucose, O-GlcNAcylation, and PKCβ-mediated MR phosphorylation are increased. Salt loading and oxidative stress also increase MR phosphorylation through the EGER/ERK pathway. PTMs inhibit ubiquitin attachment to the MR and interfere with the receptor's aldosterone-induced proteasomal degradation. Consequently, they increase the sensitivity of the MR to aldosterone and exacerbate aldosterone-associated complications.

In the original published version of this article, the following errors were introduced during the copyediting process by the Suppliers. The text originally published “In addition, the study initially included only a small number of participants.” Has been corrected to “In addition, the study should initially include a small number of participants.” The text originally published “All data requests are submitted to the corresponding author for consideration.” Has been corrected to “All data requests should be submitted to the corresponding author for consideration.” These errors bear no reflection on the article or its authors. The publisher apologizes to the authors and the readers for this unfortunate error. DOI of original article: https://doi.org/10.1016/j.ekir.2025.01.023

(Cell Reports 42, 112302; April 25, 2023) In the originally published version of this article, Figure 4 was accidentally constructed with a duplicate of panel (D) in place of the intended panel (E). The figure has been corrected online. The authors regret this error. [Formula presented] [Formula presented]

Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-024-62405-4, published online 21 May 2024 The Acknowledgements section in the original version of this Article was incomplete. “We acknowledge Dr. Hideaki Nakaya for assistance during the initial stage of this study. This study was supported by the Grants for Scientific Research (22H03091) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan and a grant from the Japan Foundation for Applied Enzymology.” now reads: "We acknowledge Dr. Hideaki Nakaya for assistance during the initial stage of this study. This study was supported by the Grants for Scientific Research (22H03091) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, the JST FOREST Program (Grant number JPMJFR210V, Japan) and a grant from the Japan Foundation for Applied Enzymology.” The original Article has been corrected.