ArticleFrontiers in bioengineering and biotechnology2024
Ultra-small curcumin-ruthenium coordination polymer nanodots prevent renal ischemia-reperfusion injury and the progression to chronic kidney disease.
Article in Frontiers in bioengineering and biotechnology, 2024. 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.
- Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis.Stem cell research & therapy · 2026Article
- Chitosan Oligosaccharide-Functionalized Ruthenium-Curcumin Nanodots for Targeted Therapy of Acute Kidney Injury.International journal of nanomedicine · 2026Article
- Nanomedicine-Driven Precision Therapy for Renal Fibrosis: From Mechanistic Insights to Kidney-Targeted Interventions.International journal of nanomedicine · 2026Review
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5 authors.
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Abstract
Renal ischemia-reperfusion (IR) induces tissue hypoxia, resulting in disrupted energy metabolism and heightened oxidative stress. These factors contribute to tubular cell damage, which is a leading cause of acute kidney injury (AKI) and can progress to chronic kidney disease (CKD). The excessive generation of reactive oxygen species (ROS) plays a crucial role in the pathogenesis of AKI. This study presents the synthesis of curcumin ultra-small coordination polymer (Ru/Cur) nanodots and their application in scavenging ROS in renal tissues. By adding ruthenium ions to a methanol solution containing the natural product curcumin, ultra-small Ru/Cur nanodots were successfully synthesized. To enhance the dispersibility of these nanoparticles in water, polyvinylpyrrolidone (PVP) was used as a growth aid, resulting in highly stable nanodots with sizes smaller than 10 nm. The results indicated that Ru/Cur nanodots effectively eliminated various ROS and demonstrated significant therapeutic effects and biocompatibility in IR-AKI mice, reducing markers of kidney function damage, alleviating renal oxidative stress, and decreasing inflammatory cell infiltration. Ru/Cur nanodots inhibited renal fibrosis by suppressing epithelial-mesenchymal transition and the secretion of transforming growth factor-β1 in the model of IR-AKI to chronic kidney disease (CKD). In summary, our findings confirm that Ru/Cur nanodots mitigate the pathological conditions associated with both AKI and its progression to CKD by reducing IR-induced tubular cell injury.
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