Skip Navigation

Cardiovascular Research 1995 30(4):511-517; doi:10.1016/S0008-6363(95)00088-7
© 1995 by European Society of Cardiology
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Duff, J. L.
Right arrow Articles by Berk, B. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Duff, J. L.
Right arrow Articles by Berk, B. C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1995, European Society of Cardiology

Angiotensin II signal transduction and the mitogen-activated protein kinase pathway

Jennifer L. Duffa, c, Mario B. Marrerob, William G. Paxtonb, Bernhard Schiefferb, Kenneth E. Bernsteina, b and Bradford C. Berk*

aDepartment of Biochemistry, Emory University, Atlanta, GA, USA
bDepartment of Pathology, Emory University, Atlanta, GA, USA
cDepartment of Medicine, Cardiology Division, University of Washington, Seattle, WA, USA

* Corresponding author. Tel. (206) 685-6960; Fax (206) 616-1580.

In this review, the angiotensin-II-mediated signal transduction pathways involved in vascular smooth muscle cell growth are discussed. Classical pathways involving phospholipase C and protein kinase C, as well as the mitogen-activated protein kinase pathway, are common signal transduction pathways activated by a variety of growth factors to stimulate cell growth. Besides its vasoconstrictor activity, angiotensin II stimulates hypertrophy of vascular smooth muscle cells and is involved in neointimal proliferation following balloon angioplasty. Understanding angiotensin-II-stimulated signaling events, as well as the crosstalk among signaling pathways, may form the basis for the development of new therapies for hypertension and restenosis.

KEYWORDS Angiotensin II; MAP kinase; Vascular smooth muscle; Hypertrophy; Signal transduction; Protein kinase C


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
A. Goette, U. Lendeckel, and H. U Klein
Signal transduction systems and atrial fibrillation
Cardiovasc Res, May 1, 2002; 54(2): 247 - 258.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
F. Jung, J. Haendeler, C. Goebel, A. M. Zeiher, and S. Dimmeler
Growth factor-induced phosphoinositide 3-OH kinase/Akt phosphorylation in smooth muscle cells: induction of cell proliferation and inhibition of cell death
Cardiovasc Res, October 1, 2000; 48(1): 148 - 157.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
M. van Bilsen
Signal transduction revisited: recent developments in angiotensin II signaling in the cardiovascular system
Cardiovasc Res, December 1, 1997; 36(3): 310 - 322.
[Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.