Breaking mitochondria and hearts

Cardiac Dysfunction Blocking the excessive mitochondrial fission mediated by dynamin-related protein 1 (Drp1) that occurs after myocardial infarction prevents cardiac dysfunction from developing. Nishimura et al. found that the cytoskeletal regulator filamin increased Drp1 activity after myocardial infarction and that the filamin-Drp1 interaction was inhibited by the U.S. Food and Drug Administration–approved drug cilnidipine (see the Focus by Boyer and Eguchi). Administering cilnidipine to mice after myocardial infarction reduced mitochondrial fission and cardiac dysfunction, suggesting that this drug could be repurposed to reduce heart attack–induced damage. Sci. Signal. 11 , eaat5185, eaav3267 (2018).