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A recent study conducted by researchers at the University of Houston explores the role of AKAP12 (A kinase anchoring protein 12) in heart failure. The study found that AKAP12 upregulation is associated with accelerated cardiac dysfunction through the AKAP12-PDE8 axis. The researchers used various methods, including live cell imaging and mouse models, to investigate the effects of AKAP12 on cardiac function. The findings suggest that AKAP12 may be a potential target for pharmacological interventions in heart failure. [Extracted from the article]

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]