Respecting boundaries: CTCF, chromatin structural organization, and heart failure

The mammalian heart is highly adaptable, responding to growth of the organism, and to the rapidly changing demands to deliver nutrients and energy throughout the body based on exercise or rest, feeding or fasting, infection, injury and other stresses. In addition to acute changes in cardiac function to meet immediate demands, the heart has an impressive capacity for remodeling in response to long-term challenges, such as the physiological hypertrophy that occurs in the athlete’s heart, as well as the pathological hypertrophy due to chronic hypertension (1).