NHLBI

Reducing heart muscle response to calcium could decrease the risk of fatal arrhythmias after heart attacks.

Vanderbilt researchers have discovered new roles for a protein involved in cell death processes that are activated to prevent tumor-causing DNA mutations.

A genetic variant that increases risk for atrial fibrillation also impacts the response to a common therapy for the heart rhythm disorder.

Diseases associated with mutations and changes in expression of the protein caveolin may result from faulty trafficking of the protein to the cell surface.

Antacids that block a certain enzyme pose a risk for a common cardiac problem in premature infants.

A factor produced by most malignant cells can both promote and inhibit tumor growth – an insight that is critical to using cancer drugs developed to block this factor.

A “profile” of the genes and regulatory networks that govern early heart valve development lay the groundwork for generating valves from a patient’s own cells.