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JCI online early table of contents: June 13, 2011
Date:6/13/2011

glycerides in mouse heart muscle cells under conditions of limited oxygen availability. Further, mice lacking VLDLR show improved survival and decreased damage to the heart following an induced heart attack. Importantly, VLDLR gene expression was found to be higher in human hearts deprived of full oxygenation compared with normal human hearts and correlated with fat accumulation. The team therefore suggests that VLDLR could provide a new target for the development of therapeutics for use in the early stages of a heart attack.

TITLE: The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

AUTHOR CONTACT:
Jan Born
Sahlgrenska University Hospital, Gteborg, Sweden.
Phone: 46.31.342.2949; Fax: 46.31.823.762; E-mail: jan.boren@wlab.gu.se.

View this article at: http://www.jci.org/articles/view/43068?key=7c3c09e53223ce76eccd


CARDIOLOGY: The protein PDE4B helps coordinate heart muscle cell contraction

Coordinated contraction of heart muscle cells is pivotal to maintaining a steady heart beat. A team of researchers, led by Rodolphe Fischmeister and Grgoire Vandecasteele, at INSERM UMR-S 769, Universit Paris-Sud, France, has now generated new insight into the molecular control of heart muscle cell contraction, information that could have a bearing on the development of new therapeutics to treat arrhythmia dysregulation of the heart rate or heart rhythm, such as beating too fast, too slow, or irregularly.

One key step in the molecular pathway that controls heart muscle cell contraction is influx of calcium (Ca2+) from outside the cell via channels known as LTCCs. LTCCs are triggered to open by increases in levels of the signaling molecule cAMP within the cell. Levels of cAMP are themselves regulated by cyclic nucleotid
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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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