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Researchers at the University of Houston College of Pharmacy have discovered that increased levels of a protein called AKAP12 in the heart can accelerate cardiac dysfunction. The researchers found that increased activity of AKAP12 reduces the contractility of cardiac myocytes, the cells responsible for heart contraction. This reduced contractility can be reversed by inhibiting an enzyme called PDE8A, which is located near AKAP12. The researchers suggest that AKAP12 could be a potential target for precision pharmacology in the treatment of heart failure, a condition that affects over 6 million adults in the United States. [Extracted from the article]