Observational studyScientific reports2018
Wnt4 is significantly upregulated during the early phases of cisplatin-induced acute kidney injury.
Observational study in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Hypoxia-Inducible Factor-1α Drives Cellular Senescence via Autophagy Activation to Promote Acute Kidney Injury-to-CKD Transition.American journal of nephrology · 2026Article
- Local Surgicel/rhBMP-7 delivery is associated with renal repair responses after surgically induced acute kidney injury.Frontiers in medicine · 2026Article
- Verbenalin attenuates renal tubular epithelial ferroptosis in ischemia-reperfusion injury induced AKI by regulating the HIF-1α/HO-1 signaling pathway.BMC nephrology · 2025Article
- Enhanced reno-protective effects of CHIR99021 modified mesenchymal stem cells against rat acute kidney injury model.BioImpacts : BI · 2025Article
- Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway.Experimental and therapeutic medicine · 2023Article
- Bioinformatics analysis of pathways of renal infiltrating macrophages in different renal disease models.Translational andrology and urology · 2021Article
- Roles and action mechanisms of WNT4 in cell differentiation and human diseases: a review.Cell death discovery · 2021Review
- Wnt signaling in kidney: the initiator or terminator?Journal of molecular medicine (Berlin, Germany) · 2020Review
- Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2019Review
- Stem cell proliferation is induced by apoptotic bodies from dying cells during epithelial tissue maintenance.Nature communications · 2019Article
- Loss of Wnt4 expression inhibits the odontogenic potential of dental pulp stem cells through JNK signaling in pulpitis.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Wnt4 is a secreted growth factor associated with renal tubulogenesis. Our previous studies identified that renal and urinary Wnt4 are upregulated following ischemia-reperfusion injury in mice, but the roles of Wnt4 in other forms of acute kidney injury (AKI) remain unclear. Here, we investigated the changes in Wnt4 expression using a cisplatin-induced AKI model. We found that renal and urinary Wnt4 expression increased as early as 12 hours, peaked at day 4 following cisplatin-induced AKI and was closely correlated with histopathological alterations. By contrast, the serum creatinine level was significantly elevated until day 3, indicating that Wnt4 is more sensitive to early tubular injury than serum creatinine. In addition, renal Wnt4 was co-stained with aquaporin-1 and thiazide-sensitive NaCl cotransporter, suggesting that Wnt4 can detect both proximal and distal tubular injuries. These data were further confirmed in a clinical study. Increased urinary Wnt4 expression was detected earlier than serum creatinine and eGFR in patients with contrast-induced AKI after vascular intervention. This study is the first to demonstrate that increased expression of renal and urinary Wnt4 can be detected earlier than serum creatinine after drug-induced AKI. In particular, urinary Wnt4 can potentially serve as a noninvasive biomarker for monitoring patients with tubular injury.
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Registered trials
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