Arrhythmias: how the mitochondria can break the heart
In a paper appearing online on November 10 in advance of print publication of the December issue of the Journal of Clinical Investigation, Brian O'Rourke and colleagues from Johns Hopkins University describe how failure of the mitochondrial network at the muscle-cell level leads to differential electrical excitability in hearts subjected to ischemia and reperfusion.
This work introduces a new mechanism to explain post-ischemic arrhythmias, in which disturbed mitochondrial function in clusters of cells in the reperfused heart leads to regional current sinks that prevent propagation.
The authors show that stabilizing mitochondrial membrane potential stabilizes the cellular action potential (AP), blunts AP shortening during ischemia, and prevents ventricular arrhythmias during reperfusion. This work could explain ischemia-related arrhythmias and explores the therapeutic potential of a compound targeting the mitochondria.
TITLE: The mitochondrial origin of post-ischemic arrhythmias
Johns Hopkins University, Baltimore, MD USA
View the PDF of this article at: https://www.the-jci.org/article.php?id=25371
Reversing obesity and diabetes works when leptin signaling is on the brain
Leptin is a hormone derived from fat cells, and defects in leptin signaling leads to obesity, overeating, and decreased energy output. Leptin signals through the leptin receptor, LEPR.
In a paper appearing online on November 10 in advance of print publication of the December issue of the Journal of Clinical Investigation, Streamson Chua and colleagues use transgenic mice to
Contact: Stacie Bloom
Journal of Clinical Investigation