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      Correction to: METTL14 promotes glomerular endothelial cell injury and diabetic nephropathy via m6A modification of α‑klotho

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      Molecular Medicine
      BioMed Central

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          Abstract

          Correction to: Mol Med (2021) 27:106 10.1186/s10020-021-00365-5 Following publication of the original article (Li et al. 2021), the authors identified an error in Fig. 2. The correct Fig. 2 is given in this erratum. Fig. 2 METTL14 promoted high glucose-induced glomerular endothelial cell injury. A Expression of METTL14 was examined by qRT-PCR after transfected with Vector or MELLT14 plasmid. **P < 0.01 vs. Vector. B Expression of METTL14 was examined by qRT-PCR after transfected with si-ctrl or MELLT14 siRNA. **P < 0.01 vs. si-Ctrl. C–E The levels of ROS, TNF-α and IL-6 were detected by ELISA. F Cell proliferation was assessed by CCK-8. G, H Cell apoptosis was analysed by TUNEL staining, Scale bar: 50 μm. *P < 0.05, **P < 0.01 vs. NG; #P < 0.05, ##P < 0.01 vs. HG + Vector; &P < 0.05, &&P < 0.01 vs. HG + si-Ctrl. Data are presented as the mean ± SD (n = 3) The original article has been corrected.

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          METTL14 promotes glomerular endothelial cell injury and diabetic nephropathy via m6A modification of α-klotho

          Background N6-Methyladenosine (m6A) modification has been implicated in many bioprocesses. However, its functions in diabetic nephropathy (DN) have not been determined. Here, we investigated the role of METTL14, a key component of the m6A methyltransferase complex, in DN. Methods The expression of METTL14 was detected in DN patients and human renal glomerular endothelial cells (HRGECs). In vitro and in vivo experiments were performed to explore the functions of METTL14 on high glocse-induced HRGECs and renal injury of DN mice. We also investigated whether METTL14 works by regulating α-klotho expression through m6A modification. Results METTL14 were highly expressed in kidneys of DN patients and high glocse-induced HRGECs both at the mRNA and protein level. Overexpression of METTL14 increased ROS, TNF-α and IL-6 levels and apoptosis in HRGECs. Conversely, METTL14 silence decreased the levels of ROS, TNF-α and IL-6 and cell apoptosis. We confirmed that METTL14 down-regulated α-klotho expression in an m6A-dependent manner. In addition, we also found that METTL14 aggravated renal injury and inflammation of db/db mice, which could partially rescued by α-klotho. Conclusion Our data revealed that METTL14 plays a vital role in high glucose-induced glomerular endothelial cells and diabetic nephropathy through m6A modification of α-klotho.
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            Contributors
            gaosi_xu@126.com
            Journal
            Mol Med
            Mol Med
            Molecular Medicine
            BioMed Central (London )
            1076-1551
            1528-3658
            24 January 2022
            24 January 2022
            2022
            : 28
            : 8
            Affiliations
            GRID grid.412455.3, ISNI 0000 0004 1756 5980, Department of Nephrology, , The Second Affiliated Hospital to Nanchang University, ; No. 1, Minde Road, Donghu District, Nanchang, 330006 China
            Author information
            https://orcid.org/0000-0001-7845-4043
            Article
            437
            10.1186/s10020-022-00437-0
            8787925
            35073839
            aef3ac51-2dee-4c3f-86c8-32db8774defe
            © The Author(s) 2022

            Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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