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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1954.)
© 2003 American Heart Association, Inc.

Editorials

Heparin and Angiogenesis

Size Matters!

Janusz Rak; Jeffrey I. Weitz

From the Henderson Research Centre, McMaster University, Hamilton, Ontario, Canada.

Correspondence to Dr Jeffrey Weitz, Henderson Research Centre, 711 Concession St, Hamilton, Ontario, L8V 1C3, Canada. E-mail jweitz@thrombosis.hhscr.org

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

Deciphering the cryptic macromolecular messages that regulate the state of the vasculature is challenging. One of the ongoing questions is the role of heparan sulfate proteoglycans (HSPG) in such processes as hemostasis, vascular remodeling, inflammation, and angiogenesis.¹ This is important because heparin preparations, the medicinal counterparts of HSPG, are cornerstones for prevention and treatment of thrombosis. Heparin preparations have evolved in recent years with the introduction of heparin fractions with reduced molecular weight. Low-molecular-weight heparin (LMWH) has a longer half-life than unfractionated heparin (UFH) and produces a more predictable anticoagulant response, properties that explain why LMWH is gradually replacing UFH for most clinical indications. What is unknown, however, is how refinements designed to improve the anticoagulant properties of heparin affect other heparin activities, such as its interaction with heparin-binding proangiogenic growth factors and their receptors.

See page 2110

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Khorana and colleagues² provide insight into this question. This study builds on the observations that (a) meta-analyses of clinical trials comparing heparin with LMWH for treatment of venous thromboembolism indicate improved survival in cancer patients given LMWH, and (b) proangiogenic growth factors, such as basic fibroblast growth factor (bFGF) and certain isoforms of vascular endothelial growth factor (VEGF), bind heparin, a property that can modulate their bioavailability and their interactions with high-affinity receptors.^1–3 Using in vitro assays of bFGF-induced angiogenesis, Khorana et al² examined the effects of an array of heparin fractions with mean molecular weights ranging from 1.7 kDa to 14 . . . [Full Text of this Article]