Mutant Phosphodiesterase 3A Protects From Hypertension-Induced Cardiac Damage

Abstract

Although in vascular smooth muscle, <i>PDE3A</i> mutations cause hypertension, they confer protection against hypertension-induced cardiac damage in hearts. Nonselective PDE3A inhibition is a final, short-term option in heart failure treatment to increase cardiac cAMP and improve contractility. Our data argue that mimicking the effect of <i>PDE3A</i> mutations in the heart rather than nonselective PDE3 inhibition is cardioprotective in the long term. Our findings could facilitate the search for new treatments to prevent hypertension-induced cardiac damage.