Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease
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 stu...
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Nature Portfolio
2025-02-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-025-88752-4 |
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| author | Hailin Li Lemei Hu Changqing Zheng Ying Kong Ming Liang Quhuan Li |
| author_facet | Hailin Li Lemei Hu Changqing Zheng Ying Kong Ming Liang Quhuan Li |
| author_sort | Hailin Li |
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| description | 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. |
| format | Article |
| id | doaj-art-8cde713d60c44602a02148b1d8515661 |
| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Nature Portfolio |
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| series | Scientific Reports |
| spelling | doaj-art-8cde713d60c44602a02148b1d85156612025-02-09T12:29:26ZengNature PortfolioScientific Reports2045-23222025-02-0115111610.1038/s41598-025-88752-4Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney diseaseHailin Li0Lemei Hu1Changqing Zheng2Ying Kong3Ming Liang4Quhuan Li5School of Biology and Biological Engineering, South China University of TechnologyDepartment of Nephrology, the Second Affiliated Hospital, School of Medicine, South China University of TechnologySchool of Biology and Biological Engineering, South China University of TechnologySchool of Biology and Biological Engineering, South China University of TechnologySchool of Medicine, South China University of TechnologySchool of Biology and Biological Engineering, South China University of TechnologyAbstract 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.https://doi.org/10.1038/s41598-025-88752-4Acute kidney injuryChronic kidney diseaseIschemia-reperfusion injuryMaladaptive repairAnkrd1 |
| spellingShingle | Hailin Li Lemei Hu Changqing Zheng Ying Kong Ming Liang Quhuan Li Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease Scientific Reports Acute kidney injury Chronic kidney disease Ischemia-reperfusion injury Maladaptive repair Ankrd1 |
| title | Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| title_full | Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| title_fullStr | Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| title_full_unstemmed | Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| title_short | Ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| title_sort | ankrd1 as a potential biomarker for the transition from acute kidney injury to chronic kidney disease |
| topic | Acute kidney injury Chronic kidney disease Ischemia-reperfusion injury Maladaptive repair Ankrd1 |
| url | https://doi.org/10.1038/s41598-025-88752-4 |
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