Abstract

Vascular calcification associated with chronic kidney disease (CKD) is an active, regulated process. Apoptosis of vascular smooth muscle cells has long been known to play a major role in its pathogenesis, with apoptotic bodies derived from these cells acting as nucleating structures for calcium crystal formation and deposition. Ye etal. now show in experimental models invitro and invivo that ferroptosis can also contribute to the development of vascular calcification in CKD.

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