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JCI table of contents: Aug. 9, 2007
Date:8/13/2007

org">jeff.molkentin@cchmc.org.

Steven R. Houser
Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 707-3278; Fax: (215) 707-0170; E-mail: srhouser@temple.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=31060


CARDIOLOGY: Extent of apoptotic cell death affects risk factor for heart failure

Changes in the size, shape, and function of the heart (cardiac remodeling) contribute to the onset and progression of heart failure. Adverse cardiac remodeling occurs in mice engineered to have sustained inflammation in the heart (MHCsTNF mice) and is accompanied by increased death of the muscle cells of the heart (cardiomyocytes) by a process known as apoptosis and decreased cardiomyocyte expression of the anti-apoptotic protein Bcl-2.

In a study that appears online on August 9 in advance of publication in the September print issue of the Journal of Clinical Investigation, Douglas Mann and colleagues from Baylor College of Medicine, Houston, do not observe adverse cardiac remodeling in MHCsTNF mice engineered to constitutively express Bcl-2 in their cardiomyocytes. However, although cardiomyocyte apoptosis was decreased, it was not completely eliminated. Further analysis revealed that Bcl-2 inhibited only one pathway of apoptosis activated by the sustained inflammatory response the intrinsic apoptotic pathway of cell death. The extrinsic apoptotic pathway of cell death proceeded unchecked. These data led the authors to suggest that the extent of cardiomyocyte apoptosis is a critical factor in determining whether or not adverse cardiac remodeling occurs.

TITLE: TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways

AUTHOR CONTACT:
Douglas L. Mann
Baylor College of Medicine,
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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