This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tsutsumi, Y. Articles by Losordo, D. W. Search for Related Content PubMed PubMed Citation Articles by Tsutsumi, Y. Articles by Losordo, D. W. Related Collections Other arteriosclerosis Related Article

(Circulation. 2005;112:1248-1250.)
© 2005 American Heart Association, Inc.

Editorial

Double Face of VEGF

Yoshiaki Tsutsumi, MD, PhD; Douglas W. Losordo, MD

From the Division of Cardiovascular Research, St. Elizabeth Medical Center, Tufts University School of Medicine, Boston, Mass.

Correspondence to Douglas W. Losordo, MD, St. Elizabeth’s Medical Center of Boston, 736 Cambridge St, Boston, MA 02135. E-mail douglas.losordo@tufts.edu

Key Words: Editorials • gene therapy • growth substances

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

The Roman god Janus (Figure) was the guardian of gates and doors and was believed to represent beginnings and endings; he is hence represented by a double-faced head. He particularly presided over all that is double-edged in life and represented the transition between the primitive and civilization, between the countryside and the city, peace and war, and the growing-up of young people. The controversy over vascular endothelial growth factor’s (VEGF) role in pathologic angiogenesis and the transition from a healthy to a diseased state is thus symbolized to a certain extent by the "gatekeeper" function that Janus played in Roman mythology.

View larger version (182K): [in this window] [in a new window]   The Roman god Janus.

See p 1347

The concept of angiogenesis as a disease pathophysiology was borne out of observations made by Folkman and colleagues regarding the enhanced vascularity of tumors. Folkman "simply" noted that tumors were bloodier than surrounding healthy tissues, positing that the tumors must have an auxiliary means of augmenting vessel growth to accommodate the expansion of unhealthy tissue. The Folkman laboratory then demonstrated that tumors produced substances capable of stimulating vessel growth,¹ igniting an entirely new field of research. One of these angiogenic factors, of course, is VEGF, and the supporting role of VEGF in tumor growth has been established by the success of VEGF neutralizing antibody for the treatment of certain solid tumors in humans.^2–4 VEGF expression has also been noted in human atherosclerotic plaque.⁵ Accordingly, the notion that VEGF may also be a key component of plaque growth is grounded in . . . [Full Text of this Article]

Related Article:

Gene Transfers of Vascular Endothelial Growth Factor-A, Vascular Endothelial Growth Factor-B, Vascular Endothelial Growth Factor-C, and Vascular Endothelial Growth Factor-D Have No Effects on Atherosclerosis in Hypercholesterolemic Low-Density Lipoprotein-Receptor/Apolipoprotein B48-Deficient Mice

Pia Leppänen, Suvi Koota, Ivana Kholová, Jonna Koponen, Christina Fieber, Ulf Eriksson, Kari Alitalo, and Seppo Ylä-Herttuala
Circulation 2005 112: 1347-1352. [Abstract] [Full Text]