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JCI online early table of contents: Sept. 1, 2010
Date:9/1/2010

f PDX1 could provide a way to treat diabetes.

TITLE: Pcif1 modulates Pdx1 protein stability and pancreatic beta cell function and survival in mice

AUTHOR CONTACT:
Doris A. Stoffers
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 215.573.5413; Fax: 215.898.5408; E-mail: stoffers@mail.med.upenn.edu.

View this article at: http://www.jci.org/articles/view/40440?key=5dd89705ebc349a1a8bf


CARDIOLOGY: Preemptive approach to decreasing scarring in the heart

Individuals with mutations in genes that generate proteins that make up the contractile unit of muscles (including heart muscle) can develop hypertrophic cardiomyopathy, a condition that causes the heart muscle to thicken, predisposing patients to heart failure. One characteristic of the thickened heart muscle in individuals with hypertrophic cardiomyopathy is scar tissue, which forms by a process known as fibrosis. A team of researchers, led by Jonathan Seidman, at Harvard Medical School, Boston, has now determined that the soluble factor Tgf-beta has a central role in the fibrosis that occurs in the hearts of mice with a disease that models hypertrophic cardiomyopathy. The team therefore suggests that preemptively treating individuals with the genetic mutations that can lead to hypertrophic cardiomyopathy with TGF-beta inhibitors might be warranted.

TITLE: Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-beta

AUTHOR CONTACT:
Jonathan G. Seidman
Harvard Medical School, Boston, Massachusetts, USA.
Phone: 617.432.7871; Fax: 617.432.7832; E-mail: seidman@genetics.med.harvard.edu.

View this article at:

Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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