The mammalian heart, the body's largest energy consumer, has evolved robust mechanisms
to tightly couple fuel supply with energy demand across a wide range of physiologic and
pathophysiologic states, yet, when compared with other organs, relatively little is known
about the molecular machinery that directly governs metabolic plasticity in the heart.
Although previous studies have defined Kruppel-like factor 15 (KLF15) as a transcriptional
repressor of pathologic cardiac hypertrophy, a direct role for the KLF family in cardiac …