Endothelin-1-induced endothelial mesenchimal transition via endothelin type B receptor stimulation: implication for chronic kidney disease

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Lariviére et al.[1], using a rat remnant kidney model of chronic kidney disease (CKD) with calcium/phosphate-rich diet associated with vitamin D supplementation, have reported that endothelin-1 plays a role in medial vascular calcification and stiffness, at least in part, through the modulation of vascular smooth muscle cell (VSMC) differentiation and vascular inflammation, thereby suggesting that endothelin-1 system may be a potential therapeutic target for improving cardiovascular morbidity in patients with CKD [1,2]. These authors have, in fact, shown that endothelin-1 production occurs not only in the endothelial cells, but also in the VSMCs, where endothelin-1 may act in an autocrine and/or paracrine manner to induce VSMC differentiation into osteoblast-like cells [1]. Moreover, the treatment with the ETA receptor subtype of endothelin-1 atrasentan prevented the expression of the osteoblastic differentiation markers BMP-2 and osteocalcin along with prevention of macrophage infiltration into the media layer and blunted expression of inflammatory cytokines [1].

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