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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Dawn, B. Articles by Bolli, R. Search for Related Content PubMed PubMed Citation Articles by Dawn, B. Articles by Bolli, R. Pubmed/NCBI databases Medline Plus Health Information Bone Marrow Transplantation Heart Attack Related Collections Angiogenesis

(Circulation. 2006;114:2203-2205.)
© 2006 American Heart Association, Inc.

Editorial

Increasing Evidence That Estrogen Is an Important Modulator of Bone Marrow–Mediated Cardiac Repair After Acute Infarction

Buddhadeb Dawn, MD; Roberto Bolli, MD

From the Institute of Molecular Cardiology, University of Louisville, Louisville, Ky.

Correspondence to Roberto Bolli, MD, Division of Cardiology, University of Louisville, Louisville, KY 40292. E-mail rbolli@louisville.edu

Key Words: Editorials • estrogen receptors • myocardial infarction • bone marrow • stem cells

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

Extensive experimental and clinical evidence accumulated over the past several years indicates that the infarcted heart can be repaired by endogenous as well as exogenous stem/progenitor cells. Experimental studies from several laboratories have reported that bone marrow–derived endothelial progenitor cells (EPCs) are mobilized after acute myocardial infarction (MI), home to the infarcted myocardium, and improve left ventricular (LV) perfusion and function.¹ Although EPCs have been shown to differentiate into a cardiomyocytic phenotype in vitro, EPC-induced beneficial effects appear to stem primarily from myocardial neovascularization. In an effort to enhance EPC-mediated cardiovascular reparative benefits, current studies are focused on the molecular mechanistic aspects of this phenomenon and on the modulation of EPC kinetics.

Article p 2261

Clinical evidence also supports an important role for EPCs in atherosclerotic cardiovascular disease. Lower numbers of colony-forming circulating EPCs are associated with an increased Framingham risk factor score and endothelial dysfunction,² and the number of circulating EPCs predicts the severity of coronary artery disease.³ These observations underscore the fact that EPCs participate not only in tissue repair after injury but also in the maintenance of endothelial integrity and function. After a stressful event such as acute MI or myocardial ischemia, additional EPCs are mobilized from the bone marrow, home to the injured tissue, and participate in neovascularization. Taken together, these considerations suggest that enhanced cardiac repair after MI may potentially be achieved by augmenting mobilization, myocardial homing, and functionality of EPCs. Elucidation of the signaling mechanisms involved in these processes is therefore important to the . . . [Full Text of this Article]

This article has been cited by other articles:

				R. Ray, C. M. Herring, T. A. Markel, P. R. Crisostomo, M. Wang, B. Weil, T. Lahm, and D. R. Meldrum Deleterious effects of endogenous and exogenous testosterone on mesenchymal stem cell VEGF production Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1498 - R1503. [Abstract] [Full Text] [PDF]