BUD23 links ribosome function with mitochondrial protein expression and efficient oxidative phosphorylation by promoting selective mRNA translation and is therefore critical to mouse development and postnatal cardiac function.
Mitochondrial-targeted SS-31 peptide ameliorates mitochondrial dysfunction and rescues pre-existing cardiac dysfunction in old mice, supporting the translational potential of mitochondrial protective interventions to treat age-related diseases.
Transgenic mice and cell models provide evidence of a pathophysiological mechanism that connects mtDNA damage to cardiac dysfunction via reduced NAD+ levels and loss of mitochondrial function and communication.
An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.
Loss and gain-of-function investigation uncovers a regulatory network controlling human heart chamber specification in which the cardiac precursor gene ISL1 accelerates ventricular induction and antagonizes retinoic acid-driven atrial commitment.
Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.