UT Southwestern researchers discovered that excessively high rates of fat burning in heart cells can damage mitochondria by depleting cardiolipin, a key lipid required for energy production. Using mouse models, they found that loss of metabolic control in fatty acid oxidation leads to enlarged, weakened hearts and heart failure-like symptoms. The study also suggests that early intervention with drugs that limit fatty acid entry into mitochondria may help prevent disease progression, though timing is critical for effectiveness.