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• W4240589788 abstract "The original article can be found online at https://doi.org/10.1038/s41374-021-00591-9. Correction to: Laboratory Investigation https://doi.org/10.1038/s41374-021-00591-9 The original version of this article unfortunately contained a mistake. Due to a typeset error the Summary was omitted. We apologize for the error. The original article has been corrected. Summary The expression of TRIM27 in MRL/lpr mice and human renal glomerular endothelial cells cultured in vitro is significantly enhanced. Down-regulating the expression of TRIM27 inhibits the loss of glycocalyx and damage to endothelial cells through the FoxO1 pathway. In addition, inhibition of the protein kinase B (Akt) pathway can reduce the damage by mediating the expression of TRIM27. TRIM27 contributes to glomerular endothelial cell injury in lupus nephritis by mediating the FoxO1 signaling pathwayLaboratory InvestigationVol. 101Issue 8PreviewTripartite motif-containing 27 (TRIM27) belongs to the triple motif (TRIM) protein family, which plays a role in a variety of biological activities. Our previous study showed that the TRIM27 protein was highly expressed in the glomerular endothelial cells of patients suffering from lupus nephritis (LN). However, whether TRIM27 is involved in the injury of glomerular endothelial cells in lupus nephritis remains to be clarified. Here, we detected the expression of the TRIM27 protein in glomerular endothelial cells in vivo and in vitro. Full-Text PDF Open Archive" @default.
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• W4240589788 date "2021-08-01" @default.
• W4240589788 modified "2023-09-30" @default.
• W4240589788 title "Correction: TRIM27 contributes to glomerular endothelial cell injury in lupus nephritis by mediating the FoxO1 signaling pathway" @default.
• W4240589788 doi "https://doi.org/10.1038/s41374-021-00602-9" @default.
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