Key result
Calcific aortic valve disease currently lacks clinically used anti-calcification drugs, highlighting the need for better mechanistic understanding to develop non-surgical therapeutic options.
This editorial highlights the discovery of DUSP26 as a mechanistic regulator of aortic valve calcification, offering potential new therapeutic targets for calcific aortic valve disease.
This editorial refers to ‘DUSP26 induces aortic valve calcification by antagonizing MDM2-mediated ubiquitination of DPP4 in human valvular interstitial cells’, by Y. Wang et al., doi:10.1093/eurheartj/ehab316. Calcific aortic valve disease (CAVD) contributes to heart valve failure, leading to over 100,000 deaths annually with a global estimate of 1.6 million CAVD patients in 2017.1 Despite the vast disease burden there are currently no clinically used anti-calcification drugs, and CAVD treatment is limited to surgical or transcatheter valve replacement. Valve replacement is a life-saving procedure, but it is not an option for all CAVD patients, and it can come with medical complications and the need for further interventions. Moreover, it is not widely available in underdeveloped countries, thus leaving many patients with no medical help. The lack of mechanistic understanding of CAVD results in the lack of therapeutic options. Obtaining a better understanding of key regulatory mechanisms in...
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Rogers et al. (2021) conducted an editorial in Calcific aortic valve disease. Calcific aortic valve disease currently lacks clinically used anti-calcification drugs, highlighting the need for better mechanistic understanding to develop non-surgical therapeutic options.
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