ArticleMedComm2025
Butyrolactone I blocks the transition of acute kidney injury to chronic kidney disease in mice by targeting JAK1.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Melanocortin 1 Receptor Signaling Protects Against Tubular Epithelial Cell Injury and M1 Macrophage Polarization in Acute Kidney Injury.Integrative zoology · 2026Article
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Renal Tubular Epithelial CRLF1 Interacts With ITGB1 to Accelerate Fibrosis During the Transition From AKI to CKD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptomics reveal dysregulated genes during folic acid-induced acute injury and fibrosis in kidney and their attenuation by antioxidantAmerican journal of physiology. Cell physiology · 2026Article
- Yuanhuacine modulates lipopolysaccharide-induced interleukin-6 through regulation of the JAK1/STAT3 pathway and prevents tubular damage in acute kidney injury.Experimental and therapeutic medicine · 2025Article
- Butyrolactone I blocks the transition of acute kidney injury to chronic kidney disease in mice by targeting JAK1.MedComm · 2025Article
- Huangkui capsule combined with finerenone attenuates diabetic nephropathy by regulating the JAK2/STAT3 signaling pathway based on network pharmacology, molecular docking, and experimental verification.Frontiers in pharmacology · 2025Article
- Anthraquinones fromDrug design, development and therapy · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is a disease that affects more than 850 million people. Acute kidney injury (AKI) is a common cause of CKD, and blocking the AKI-CKD transition shows promising therapeutic potential. Herein, we found that butyrolactone I (BLI), a natural product, exerts significant nephroprotective effects, including maintenance of kidney function, inhibition of inflammatory response, and prevention of fibrosis, in both folic acid- and ureteral obstruction-induced AKI-CKD transition mouse models. Notably, BLI showed greater blood urea nitrogen reduction and anti-inflammatory effects than telmisartan. Bioinformatics analysis and target confirmation assays suggested that BLI directly binds to JAK1, and kinase inhibition assay confirmed it is a potent JAK1inhibitor with an IC
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