Key result
Parathyroid hormone activates valvular endothelial-to-mesenchymal transition via the miR-29a-5p/GSAP/Notch1 pathway, contributing to valvular calcification in CKD rats.
Why the study?
Few studies had investigated EndMT in CKD-induced valvular calcification, and whether PTH induces valvular EndMT along with its underlying mechanism required determination.
This preclinical study identifies the miR-29a-5p/GSAP/Notch1 pathway as a key mechanism by which parathyroid hormone induces endothelial-to-mesenchymal transition and subsequent valvular calcification in chronic kidney disease.
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PTH may drive valvular EndMT and calcification in CKD; leaves open whether miR-29a/Notch1 inhibition alters clinical outcomes.
Wang et al. (2021) studied Valvular calcification in chronic kidney disease. Parathyroid hormone (PTH) vs. Control was evaluated on Valvular endothelial-to-mesenchymal transition and calcification. Parathyroid hormone activates valvular endothelial-to-mesenchymal transition via the miR-29a-5p/GSAP/Notch1 pathway, contributing to valvular calcification in CKD rats.
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