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JCI table of contents: June 21, 2007

study appearing online on June 21 in advance of publication in the July print issue of the Journal of Clinical Investigation, Joseph Hill and colleagues from the University of Texas Southwestern Medical Center examine the role of autophagy the tightly regulated recycling of cellular products leading to programmed cell death in heart failure. The authors found that pressure overload of the heart greatly increased cardiac autophagy and heart failure in mice. Furthermore, disruption of the gene encoding the protein Beclin1, a protein known to be required for autophagy, decreased cardiac muscle cell autophagy and diminished harmful structural changes to the heart under severe pressure stress. Conversely, Beclin 1 overexpression increased autophagy activity and the severity of harmful structural changes in the hearts of these animals. Taken together, the data implicate autophagy in the development of pressure/load-induced heart failure and as such it may be a target for novel therapeutic intervention.

Title: Cardiac autophagy is a maladaptive response to hemodynamic stress

Author Contact:

Joseph A. Hill
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone : (214) 648-1400; Fax: (214) 648-1450; E-mail: joseph.hill@utsouthwestern.edu

View the PDF of this article at: http://www.the-jci.org/article.php?id=27523


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Glaucoma, a leading cause of irreversible blindness in the United States, usually occurs when increased fluid pressure in the eye damages the optic nerve. However, in a significant subset of glaucomas elevated intraocular pressure (IOP) is not a symptom [e.g. in normal tension glaucoma (NTG)] and in other cases a reduction in IOP does not prevent disease progression. In a
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
21-Jun-2007


Page: 1 2 3 4 5 6 7

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