Beverly A. Rothermel

TL;DR: Findings implicate autophagy in the pathogenesis of load-induced heart failure and suggest it may be a target for novel therapeutic intervention.

TL;DR: It is concluded that the neonatal mammalian heart can regenerate after myocardial infarction through proliferation of preexisting cardiomyocytes and that the miR-15 family contributes to postnatal loss of cardiac regenerative capacity.

TL;DR: It is shown that reactive oxygen species (ROS), oxidative DNA damage, and DNA damage response (DDR) markers significantly increase in the heart during the first postnatal week, revealing a protective mechanism that mediates cardiomyocyte cell-cycle arrest in exchange for utilization of oxygen-dependent aerobic metabolism.

TL;DR: It is shown that, during the onset of ER stress, the reticular and mitochondrial networks are redistributed towards the perinuclear area and their points of connection are increased in a microtubule-dependent fashion, which establishes the metabolic basis for the adaptation to this response.

TL;DR: A small family of proteins, termed MCIP1 and MCIP2 (for myocyte-enrichedcalcineurin interacting protein), that are expressed most abundantly in striated muscles and that form a physical complex with calcineURin A, which may modulate calcineurIn-dependent pathways that control hypertrophic growth and selective programs of gene expression in Striated muscles.