Semin Nephrol. 2026 Sep 3:151717. doi: 10.1016/j.semnephrol.2026.151717. Online ahead of print.
ABSTRACT
Vascular calcification (VC) is a major independent risk factor for cardiovascular events in patients with chronic kidney disease (CKD), yet no effective clinical treatment is currently available. Quercetin, a natural flavonoid abundant in fruits and vegetables, demonstrates promising therapeutic potential in CKD-related VC (CKD-VC). This review systematically summarizes the molecular mechanisms by which quercetin ameliorates CKD-VC from two principal aspects: directly targeting the vascular smooth muscle cells (VSMCs) phenotypic transition and indirectly alleviating the procalcification microenvironment. At the cellular level, quercetin inhibits osteoblastic transdifferentiation, restores calcium-phosphorus homeostasis, enhances calcification inhibitor expression, and effectively alleviates pathologic processes, including oxidative stress, inflammation, cellular senescence, and apoptosis, while also regulating epigenetic modifications. In terms of the procalcification microenvironment, quercetin mitigates CKD-VC by improving gut microbiota dysbiosis, reducing uremic toxin accumulation, protecting endothelial barrier function, and inhibiting ferroptosis. In conclusion, based on existing research evidence, quercetin demonstrates the potential to exert anticalcification effects through multitarget and multipathway mechanisms.
PMID:42692942 | DOI:10.1016/j.semnephrol.2026.151717