文档介绍：Inhibition of cardiac fibroblast proliferation and myofibroblast differentiation by resveratrol
Presenter: W Yang
2010-11
Origin
BY:
Erik ,1 Jennifer ,1 Xiaojin Zhang,1 Joshua ,2 and Meszaros1.
FROM:
Am J Physiol Heart Circ Physiol 288:H1131–H1138,2005.
IF=
① Background
② Suppose
③ Methods
④ Results
⑤ Conclusion
Background
Cardiac fibroblasts(CFs) regulate myocardial remodeling by proliferating,differentiating,and secreting extracellular matrix proteins.
Prolonged activation of CFs leads to cardiac fibrosis and reduced myocardial contractile function.
Prolonged activation of CFs is a direct consequence of hypertension and heart failure and leads to cardiac fibrosis,a
condition characterized by excess ECM deposition and a stiff
myocardium.
(CFs)are the predominant secretory cells of extracellular matrix(ECM)proteins in the heart and the key mediators of normal and pathological cardiac remodeling.
ANG II levels are elevated during hypertension and heart
peptide hormone has direct and potent effects on CF function,including activation of the mitogen-activated
protein kinase (MAPK)/extracellular signal-regulated kinase
(ERK) cascade and cellular proliferation via direct stimulation of the ANG II type1(AT1) have demonstrated that proliferation of CFs is dependent on ERK kinase (MEK) and ERK1/2 activation via pharmacological inhibition of MEK.
In addition to activating ERK,ANG II regulates collagen type I expression,at least in part,by inducing CFs to produce and secrete transforming growth factor-β.
TGF-βis a potent paracrine mediator of differentiation and contributes to the development of cardiac fibrosis by increasing the number of myofibroblasts in the heart.
Resveratrol(RES;trans-3,4,5 trihydroxystilbene),a phytoalexin found in the skins of grapes,has been identified as a key biologically active ingredient in red wine.
RES has been credited with mediating a number of beneficial effe