JCI table of contents: May 10, 2007

vard Medical School, Boston, Massachusetts, USA.
Phone : (617) 278-6617; Fax : (617) 278-3368; E-mail : bergmeier@cbrinstitute.org

View the PDF of this article at: https://www.the-jci.org/article.php?id=30575


Protecting the heart against mechanical stress

Enlargement or overgrowth of heart cells known as cardiomyocytes cardiac hypertrophy is a common event in many heart diseases, and occurs in an effort to restore stresses on the heart wall to normal levels. A protein called ST2 that is produced by cardiomyocytes is a potentially useful biomarker in heart diseases, however its role in heart disease has been unclear. In a study appearing online on May 10 in advance of publication in the June print issue of the Journal of Clinical Investigation, Richard Lee and colleagues from Harvard Medical School show that ST2 and its recently identified ligand IL-33 work together to protect the heart in times of cardiac stress.

The authors showed that deletion of ST2 in mice increased cardiac hypertrophy as well as the thickening and scarring of heart tissue, and decreased survival of these animals in response to cardiac stress. Administration of IL-33, which is made by cells called fibrbroblasts, improved pathological changes and survival in response to cardiac stress in mice with intact ST2, but not in ST2-/- mice. The study suggests that IL-33/ST2 signaling is a crucial mechanism for protecting the heart and shows that cardiomyocytes and cardiac fibroblasts signal to each other in times of cardiac stress.

TITLE: IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system

Richard Lee
Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Phone : (617) 768-8272; Fax: (61

Contact: Brooke Grindlinger
Journal of Clinical Investigation

Page: 1 2 3 4 5

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