Heart failure drugs may work within days by boosting cells' energy supply

Researchers have discovered that SGLT2 inhibitors, drugs initially developed for diabetes treatment and often prescribed for heart failure, function by activating a crucial enzyme called PANK1 within heart cells. This activation enhances the heart cells' capacity to produce and utilize energy, a discovery that could potentially lead to new treatments for heart failure.

The study, conducted by researchers at the University of Pennsylvania's Perelman School of Medicine and published in Science, reveals that SGLT2 inhibitors boost production of coenzyme A (CoA), a molecule vital for converting nutrients into energy. The improved CoA production leads to better heart cell contractions and relaxations, which are impaired in heart failure patients.

Researchers identified PANK1 as the direct target of these medications, and activating this pathway improves heart cell function, potentially explaining the rapid benefits patients often experience from these drugs. The study's findings suggest that PANK1 activation may be a major driver of the drugs' effectiveness, and could also help explain why heart failure patients often see improvements within days of starting treatment.

The research opens up possibilities for developing new drugs that directly target PANK1, which could provide the heart benefits of SGLT2 inhibitors while potentially reducing associated side effects.