AJP - Heart Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 294: H1971-H1977, 2008. First published March 28, 2008; doi:10.1152/ajpheart.91503.2007
0363-6135/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/5/H1971    most recent
91503.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Moens, A. L.
Right arrow Articles by Kass, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Moens, A. L.
Right arrow Articles by Kass, D. A.

INVITED REVIEW

Mechanisms and potential therapeutic targets for folic acid in cardiovascular disease

An L. Moens,1,2 Christiaan J. Vrints,2 Marc J. Claeys,2 Jean-Pierre Timmermans,2 Hunter C. Champion,1 and David A. Kass1

1Johns Hopkins Medical Institutions, Division of Cardiology, Baltimore, Maryland; and 2University of Antwerp, Division of Cardiology, Antwerp, Belgium

Folic acid (FA) is a member of the B-vitamin family with cardiovascular roles in homocysteine regulation and endothelial nitric oxide synthase (eNOS) activity. Its interaction with eNOS is thought to be due to the enhancement of tetrahydrobiopterin bioavailability, helping maintain eNOS in its coupled state to favor the generation of nitric oxide rather than oxygen free radicals. FA also plays a role in the prevention of several cardiac and noncardiac malformations, has potent direct antioxidant and antithrombotic effects, and can interfere with the production of the endothelial-derived hyperpolarizing factor. These multiple mechanisms of action have led to studies regarding the therapeutic potential of FA in cardiovascular disease. To date, studies have demonstrated that FA ameliorates endothelial dysfunction and nitrate tolerance and can improve pathological features of atherosclerosis. These effects appear to be homocysteine independent but rather related to their role in eNOS function. Given the growing evidence that nitric oxide synthase uncoupling plays a major role in many cardiovascular disorders, the potential of exogenous FA as an inexpensive and safe oral therapy is intriguing and is stimulating ongoing investigations.

endothelial nitric oxide synthase; uncoupling; superoxide; tetrahydrobiopterin; homocysteine


Address for reprint requests and other correspondence: A. L. Moens, Univ. Hospital of Antwerp, Div. of Cardiology, Wilrijkstraat 10, 2650 Antwerp-Edegem, Belgium (e-mail: an.moens{at}uza.be)




This article has been cited by other articles:


Home page
 Eur Heart JHome page
C. Antoniades, A. S. Antonopoulos, D. Tousoulis, K. Marinou, and C. Stefanadis
Homocysteine and coronary atherosclerosis: from folate fortification to the recent clinical trials
Eur. Heart J., January 1, 2009; 30(1): 6 - 15.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.