For patients with a diseased heart, everyday tasks like climbing a flight of stairs or walking across a room eventually become exhausting. 

Regardless of the underlying cause of the damage, heart disease typically progresses due to a constant barrage of oxidative stress and toxic lipids that ultimately impact the ability of the heart to function normally.
Oxidative stress occurs when harmful oxygen-containing molecules outnumber helpful antioxidants, leading to damaging reactions with proteins, DNA and other cell components. 

Now, two new studies by researchers at the Lewis Katz School of Medicine demonstrate that a molecule in the heart called Krϋppel-like factor (KLF)-5 is responsible for increasing heart dysfunction by single-handedly fueling both the generation of injurious oxidizing molecules and the accumulation of toxic lipids in the heart. 

The studies are the first to identify KLF5 as a key contributor to cardiac damage in animal models. 

“Our findings expose KLF5 as a new target for different types of cardiac disease,” said Konstantinos Drosatos, associate professor of pharmacology at the Center for Translational Medicine, the Center for Metabolic Disease Research and the Alzheimer’s Center at Temple. “As a unifying factor driving oxidative stress and accumulation of toxic lipids in the heart, the implications of targeting KLF5 could be far-reaching, opening up treatment for a broad range of diseases involving heart dysfunction.”

The studies were funded in part by the National Heart Lung and Blood Institute of the National Institutes of Health, the National Institute of General Medical Sciences, the W. W. Smith Charitable Trust and the American Heart Association.

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