Abstract

Choi et al demonstrated that dipeptidyl peptidase-4 (DPP-4, also known as CD26), increased valvular calcification and promoted calcific aortic valve disease progression. They found that nitric oxide depletion in human valvular endothelial cells activated nuclear factor-κB in human valvular interstitial cells. Consequently, activated nuclear factor-κB promoted DPP-4 expression, which then induced osteogenic differentiation of valvular interstitial cells by limiting autocrine insulin-like growth factor-1 signaling.1 Calcific aortic valve disease (CAVD) is a progressive accumulation of fibrocalcific matrices and calcified, bony nodules in aortic valves. It causes aortic stenosis accounting for ≈50% of cardiac valve disease. In the developed countries, CAVD is the third most common cardiovascular disease behind coronary artery …

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