ArticleScientific reports2025
Prostaglandin E2 receptor EP4 activation induces tolerogenic dendritic cells to mitigate ischemic acute kidney injury.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Multimodal biomarker approach using urinary prostaglandin E2, kidney injury molecule-1 and resistive index for assessing kidney adaptation in transplant recipients.BMC nephrology · 2026Article
- Molecular mechanisms of acute inflammation: systemic responses and kidney-specific pathophysiology.Function (Oxford, England) · 2026Review
- Combining spatial and single-cell transcriptome data to analyze tertiary lymphoid structures in clear cell renal cell carcinoma reveals prognostic biomarkers.Journal of translational medicine · 2026Article
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11 authors.
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Abstract
The prevalence and mortality rates of acute kidney injury (AKI) remain high, with ischemia-reperfusion (I/R) being a major cause in clinical settings. Dendritic cells (DCs) play a crucial role in inducing the infiltration of inflammatory cells into the kidneys during I/R, leading to persistent kidney damage. However, immature DCs (imDCs) maintain self-tolerance under homeostatic conditions. Therefore, targeting the immunomodulatory duality of DCs to prevent I/R-AKI is of significant importance. In this study, we found Pre-treatment of bone marrow-derived dendritic cells (BMDCs) with the EP4 receptor agonist L-902,688 induced the generation of EP4
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