Xiuying Bai

Abstract Medial vascular calcification is a major cardiovascular complication of chronic kidney disease (CKD), with the uremic toxin indoxyl sulfate (IS) implicated in its pathogenesis. However, the molecular mechanisms by which IS promotes vascular calcification remain incompletely understood. In human aortic smooth muscle cells (hASMCs), IS induced oxidative stress and stimulated the MEK–ERK1/2 and PI3K–AKT signaling pathways, leading to mTORC1 activation.

Corrigendum Open Access | 10.1172/JCI193400 Published in Volume 135, Issue 8 on April 15, 2025 J Clin Invest. 2025;135(8):e193400. https://doi.org/10.1172/JCI193400. © 2025 Bai et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. View PDF Abstract CYP24A1 (hereafter referred to as CYP24) enzymatic activity is pivotal in the inactivation of vitamin D metabolites.

Abstract CYP24A1 (hereafter referred to as CYP24) enzymatic activity is pivotal in the inactivation of vitamin D metabolites. Basal renal and extrarenal CYP24 is usually low but is highly induced by its substrate 1,25-dihydroxyvitamin D. Unbalanced high and/or long-lasting CYP24 expression has been proposed to underlie diseases like chronic kidney disease, cancers, and psoriasis that otherwise should favorably respond to supplemental vitamin D.