RhoA and resistance artery remodeling
Institut National de la Santé et de la Recherche Médicale U-533, Institut du Thorax, Nantes, France Submitted 16 July 2004 ; accepted in final form 25 August 2004 Resistance arteries are able to adapt to physiological and pathophysiological stimuli to maintain adequate perfusion according to the met...
Gespeichert in:
Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2005-03, Vol.288 (3), p.H1051-H1056 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Institut National de la Santé et de la Recherche Médicale U-533, Institut du Thorax, Nantes, France
Submitted 16 July 2004
; accepted in final form 25 August 2004
Resistance arteries are able to adapt to physiological and pathophysiological stimuli to maintain adequate perfusion according to the metabolic demand of the tissue. Although vasomotor control allows rapid adaptation of lumen diameter, vascular remodeling constitutes an active process that occurs in response to long-term alterations of hemodynamic parameters. Unfortunately, this initially adaptive process contributes to the pathology of vascular diseases. Recent studies have demonstrated the participation of Rho protein signaling pathways in several cardiovascular pathologies including hypertension, coronary artery spasm, effort angina, atherosclerosis, and restenosis. Functional analyses have further revealed that RhoA-dependent pathways are involved in excessive contraction, migration, and proliferation associated with arterial diseases. The present review focuses on the role of Rho proteins, in particular RhoA, in vascular smooth muscle cells and the involvement of Rho-dependent signaling pathways in resistance artery remodeling, more particularly in relation to hypertension.
signal transduction; smooth muscle; vascular diseases
Address for reprint requests and other correspondence: G. Loirand, Inserm U-533, Faculté des Sciences, 2 rue de la Houssinière, BP 92208, 44322 Nantes cedex 3, France (E-mail: gervaise.loirand{at}nantes.inserm.fr ) |
---|---|
ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/ajpheart.00710.2004 |