Decorin Gene Delivery Inhibits Cardiac Fibrosis in Spontaneously Hypertensive Rats by Modulation of Transforming Growth Factor-β/Smad and p38 Mitogen-Activated Protein Kinase Signaling Pathways

2009 ◽  
Vol 20 (10) ◽  
pp. 1190-1200 ◽  
Author(s):  
Wen Yan ◽  
Peihua Wang ◽  
Chun Xia Zhao ◽  
Jiarong Tang ◽  
Xiao Xiao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Spontaneously Hypertensive Rats ◽  
Cardiac Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mitogen Activated Protein Kinase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Mitogen Activated Protein ◽  
Protein Kinase Signaling

Prophylactic effects of an N- and L-type Ca2+ antagonist, cilnidipine, against cardiac hypertrophy and dysfunction in stroke-prone, spontaneously hypertensive rats

2005 ◽  
Vol 83 (8-9) ◽  
pp. 785-790 ◽  
Author(s):  
Kumiko Takemori ◽  
Hiroyuki Ishida ◽  
Kensaku Dote ◽  
Kazuo Yamamoto ◽  
Hiroyuki Ito
Keyword(s):  
Growth Factor ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Fibroblast Growth ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Beneficial Effects

To clarify the beneficial effects of cilnidipine, an L- and N-type calcium channel blocker, which were clinically observed against diastolic dysfunction in hypertrophied hearts of hypertensive patients, we investigated the effects of cilnidipine on cardiac remodeling and enhanced gene expression in stroke-prone, spontaneously hypertensive rats in comparison with that of captopril, a well-known angiotensin-converting enzyme inhibitor, at threshold doses with little blood pressure lowering effect. The expression of type III collagen and β/α-myosin heavy chain as well as transforming growth factor-β, and basic fibroblast growth factor were suppressed by both treatments, indicating the prevention or amelioration of cardiac dysfunction. Such beneficial effects were much more intense with cilnidipine treatment than in captopril. These results indicate that Ca2+ is a key factor in the pathogenesis of cardiac remodeling in hypertension. One possible beneficial effect of cilnidipine in the prevention of cardiac dysfunction may be due to the decreased amount of growth factors such as transforming growth factor-β and basic fibroblast growth factor via direct action for Ca2+ influx and also via inhibition of local renin-angiotensin system in the myocardium.Key words: hypertension, cardiac hypertrophy, Ca2+-blocker, growth factor.

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