Key result
Diabetes mellitus is a powerful risk factor for calcific aortic valve disease, potentially driving osteogenic transformation of valvular interstitial cells and representing a new therapeutic target.
This perspective highlights the mechanistic links between diabetes and calcific aortic stenosis, suggesting that targeting the osteogenic phenotype, potentially with DPPIV inhibitors, may offer a new therapeutic avenue.
Supports mechanistic research on diabetes in aortic stenosis; hypothesis-generating and should not change practice.
Calcific aortic valve stenosis (CAVD) has similar classical coshared risk factors that are associated with endothelial cell dysfunction and cardiovascular disease. For example, lifestyle habits similar to those predisposing to coronary artery disease, inflammation, hypertension, advanced age, malegender, hyperlipidemia, diabetes mellitus, cigarette smoking, metabolic syndrome, and end-stage kidney disease have all been linked with the development of CAVD. Diabetes mellitus (DM) is a powerful known risk factor for CV disease and aortic stenosis. However, mechanisms causing CAVD still remain unknown to a large extent. Pro-atherogenic factors cause amplification of vascular wall inflammation and increased endothelial oxidative stress, thereby activating aortic valve interstitial cells (cells that lie between other cells) toward anosteogenic phenotype favoring the development of CAVD in DM
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Lin et al. (2018) conducted a review in Calcific Aortic Stenosis and Diabetes Mellitus. Diabetes mellitus is a powerful risk factor for calcific aortic valve disease, potentially driving osteogenic transformation of valvular interstitial cells and representing a new therapeutic target.
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