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(Circulation Research. 2003;92:947.)
© 2003 American Heart Association, Inc.

Editorials

Angiopoietin-1 and Pulmonary Hypertension

Cause or Cure?

J.S. Rudge, G. Thurston, G.D. Yancopoulos

From Regeneron Pharmaceuticals, Inc, Tarrytown, NY.

Correspondence to George D. Yancopoulos, Regeneron Pharmaceuticals, Inc, 777 Old Saw Mill River Rd, Tarrytown, NY 10591. E-mail gdy@regpha.com

Key Words: pulmonary hypertension • angiopoietin-1 • Tie2 • vascular endothelial growth factor • smooth muscle cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Our very existence depends on the air that we breathe, as well as the remarkable systems that have evolved to ensure that the oxygen we take into our lungs is efficiently delivered to the rest of the body via the bloodstream. When these systems begin to fail, life itself can become quite tenuous. Such failure occurs in pulmonary hypertension, a rare but serious disease whose pathophysiology remains obscure and increasingly controversial, as highlighted by two recent studies.^1,2 Both studies focus on the potential role of angiopoietin-1 in this disease, but reach entirely antithetical conclusions.

The right side of the heart pumps blood into the lung vasculature, which consists of a low-resistance network that normally adjusts to increases in blood flow (eg, as necessitated by exercise) by dilation of its terminal arterioles to allow for increased flow without increasing resistance. In pulmonary hypertension, pulmonary arterial pressure is increased at rest and ratchets up dramatically with exercise, due to an inability to easily accommodate increased flow, imposing stress on the right ventricle. In response to the increased back pressure, the right side of the heart can hypertrophy to the point of failure. Current treatments are moderately effective at best. A study featured in this issue of Circulation Research,² from the laboratory of Duncan Stewart, claims that angiopoietin-1 can have dramatic protective effects in an animal model of pulmonary hypertension. On the other hand, a recent article in the New England Journal of Medicine by Thistlethwaite and colleagues¹ argues quite the opposite, . . . [Full Text of this Article]

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