Early diagnostic and prognostic potential of miR-200c in acute kidney injury
Abstract Objectives Acute kidney injury (AKI) is a serious clinical condition characterized by rapid renal dysfunction and high mortality. Although the dysregulation of microRNAs is well-established in AKI, the clinical significance of microRNA-200c in this condition remains poorly defined. Methods RT-qPCR detected miR-200c and inflammatory factors (TNF-α, IL-6, IL-8) in serum from 75 patients with AKI and 72 controls. ROC curves assessed miR-200c’s diagnostic value. Multivariate Cox regression identified independent survival risk factors. Kaplan-Meier curves analyzed miR-200c-survival links. Establishment of an in vitro cell model induced by LPS. To assess cell proliferation and apoptosis, CCK-8 assays and flow cytometry were employed. Results miR-200c expression was significantly elevated in AKI patients. Serum miR-200c effectively distinguishes AKI patients from controls. Compared with the group of patients with good prognosis, the miR-200c expression was significantly higher in the group of patients with poor prognosis. Survival analysis showed that higher miR-200c levels in AKI cases correlated with a notable decline in 90-day survival. Suppression of miR-200c expression enhanced cell proliferation, attenuated apoptosis, and reduced inflammatory factor levels, thereby ameliorating AKI progression. Conclusions miR-200c shows promising application potential in the diagnosis and prognosis assessment of AKI. Suppressing miR-200c expression effectively curbs aberrant cellular behaviors and pro-inflammatory responses.
Authors
- Jingjing Gong (ORCID: https://orcid.org/0000-0002-1756-2638)
- Zhenwen Chen
- Zijian Tian
- Feifei Wang
Institutions
- Capital Medical University (CN)
- Peking University (CN)
- Peking University People's Hospital (CN)
- Beijing Children’s Hospital (CN)
Publication Details
- Journal
- Turkish Journal of Biochemistry
- Published
- 2025-12-22
- DOI
- https://doi.org/10.1515/tjb-2025-0308
- Primary Topic
- MicroRNA in disease regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.00