Biomedicine

Aorta Not to Happen

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Science  22 Feb 2002:
Vol. 295, Issue 5559, pp. 1429
DOI: 10.1126/science.295.5559.1429a

In response to stresses such as high blood pressure and myocyte death, cardiac muscle cells can become hypertrophic (enlarged). Under continued stress, however, the ventricular wall can dilate and contract less strongly, leading to congestive heart disease. Several factors are likely to contribute to this progression, although the key mechanisms have yet to be established.

Hara et al. tested whether mast cells, which are associated with heart tissue, could influence the transition from compensatory hypertrophy to heart failure. In a model in which stress was applied by artificial constriction of the aorta, mast cell- deficient W/Wv mice were resistant to chronic systolic overload. Compared to wild-type mice, W/Wv animals exhibited less heart enlargement and perivascular fibrosis. Decreased cardiac pathophysiology also was observed after administration of the mast cell degranulation inhibitor tranilast to normal mice subject to aortic constriction. The authors suggest that mast cells could contribute to heart failure by releasing molecules such as histamine and chymase, which can promote apoptosis of myocytes and structural changes in components of cardiac tissue. —SJS

J. Exp. Med.195, 375 (2002).

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