S100A8/A9 high-expression macrophages mediate renal tubular epithelial cell damage in acute kidney injury following acute type A aortic dissection surgery.

ABSTRACT:

Background

Acute kidney injury (AKI) is a major complication after acute type A aortic dissection (ATAAD), with an incidence rate of 20-66.7%. Many patients with AKI after ATAAD surgery show no clear signs of ischemia-reperfusion injury. In our previous study, S100A8 and S100A9 were identified as predictive biomarkers of AKI after ATAAD surgery. These proteins are primarily expressed in neutrophils and macrophages, where they contribute to cell damage and immune cell activation. However, the roles of S100A8/A9 in ATAAD-associated AKI remain unclear.

Methods

In this study, transcriptomics sequence was applied to identify differentially expressed genes in renal tubular epithelial cells (TCMK-1), stimulated by culture supernatant of S100A8/A9 overexpressed and downregulated RAW

SUBMITTER: Cai X 

PROVIDER: S-EPMC12015165 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature