Journal Article Journal Article Epublish
PubMed: 39920300 DOI: 10.1038/s41598-025-88752-4
Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease.
Sci Rep 15(1):4659
Authors: Hailin Li, Lemei Hu, Changqing Zheng, Ying Kong, Ming Liang, Quhuan Li
Affiliations
- School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China.
- Department of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, People's Republic of China. School of Medicine, South China University of Technology, Guangzhou, People's Republic of China.
- School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China. School of Life Sciences, Tsinghua University, Beijing, 100084, People's Republic of China.
- School of Medicine, South China University of Technology, Guangzhou, People's Republic of China. Department of Nephrology, Guangzhou First People's Hospital, Guangzhou, People's Republic of China.
- School of Biology and Biological Engineering, South China University of Technology, Guangzhou, 510006, Guangdong, China.
Abstract
Ischemia-reperfusion injury (IRI) is one of the leading causes of acute kidney injury (AKI), predisposing patients to chronic kidney disease (CKD) due to maladaptive renal repair. Nevertheless, the molecular mechanisms and biomarkers that cause maladaptive repair remain unclear. In this study, we used single-nucleus RNA sequencing data from GEO database (GSE139107) to identify molecular markers during the transition from AKI to CKD caused by IRI. Analysis of intercellular crosstalk, trajectory and machine learning algorithms revealed hub cell clusters and genes. Proximal tubule (PT) cells, especially a new cluster (New PT2), significantly interacted with fibroblasts during the transition. The expression levels of hub genes were validated using the bulk RNA-seq data (GSE98622) and further confirmed through RT-qPCR and immunohistochemical analysis in ischemia-reperfusion injury (uIRI) mice. Ankrd1, a hub gene in New PT2, showed sustained upregulation in the proximal tubule in AKI. Compared to the sham-operated group, the expression of Ankrd1 in mice increased at 0.5 days post-reperfusion, peaked at day 1, and remained significantly elevated up to 60 days. This study indicated that the upregulation of Ankrd1 was positively associated with the progression from AKI to CKD and may potentially serve as a valuable biomarker for this transitional process.
MeSH
Kidney Diseases, Cells, Up-Regulation, Genes, Kidney, Biomarkers, Reperfusion, Reperfusion Injury, Natural Science Disciplines, Acute Kidney Injury