Erratum

Abstract

[This corrects the article DOI: 10.1159/000507117.].

Fig. 2a

Mechanisms of Zn2+-dependent HDACs in podocyte injury. The activation of HDAC induces podocyte injury by regulation of EGR1. Moreover, upregulation of HDAC4 decreases autophagy to mitigate podocyte injury by upregulating the acetylated level of STAT1. Impaired miR-29a signaling accelerates podocyte apoptosis, proteinuria, and renal fibrosis through promotion of HDAC4-dependent effects, which negatively regulates the expression of miR29a via deacetylation of H3K9. In addition, HDAC7 can reduce KLF4 expression by downregulating the H3K9ac level in the KLF4 promoter, resulting in podocyte developmental toxicity induced by PCE in male offspring rats. b Effects of deacetylation on histone mediated by Sirts in podocytes. Under normal conditions, Sirts could deacetylate the histone and then inhibit gene transcription. However, protein levels of Sirt1 and Sirt6 are downregulated in podocyte injury, and transcription is activated. For example, the decrease in Sirt1 enhances the level of histone acetylation on H3 and H4, leading to a reduction in histone methylation of H3K9, which then promotes Claudin-1 transcription and ultimately causes podocyte injury. In addition, Sirt6 protects against podocyte injury and proteinuria in DN and focal segmental glomerulosclerosis, at least in part through epigenetic regulation of Notch signaling via binding to their promoters and deacetylating H3K9. c Effects of deacetylation on nonhistone mediated by Sirts in podocytes. Sirt1 regulates deacetylation of PGC-1α and cortactin and then improves mitochondrial function and maintains the cytoskeleton. Moreover, Sirt1 could also deacetylate FOXO3, FOXO4, p65 NF-kB, and STAT3, followed by attenuation of podocyte injury via anti-inflammation, antiapoptosis, reduction of oxidative stress, and inhibition of senescence. In addition, recent studies have demonstrated that colocalization of Sirt3 and KLF15 leads to deacetylation of KLF15, with decreased expression of fibrosis factors in podocytes with AngII treatment.