Is Smad3 the key to inflammation and fibrosis in hypertensive heart disease?

Hypertension

Volumn 55, Issue 5, 2010, Pages 1088-1089

  Graf, Kristof ^a,b   Schaefer Graf, Ute M ^b  

^a Judisches Krankenhaus Berlin   (Germany)

^b St Joseph Hospital   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

MONOCYTE CHEMOTACTIC PROTEIN 1; SMAD3 PROTEIN; TRANSFORMING GROWTH FACTOR BETA;

HEART EJECTION FRACTION; HEART FAILURE; HEART INFARCTION SIZE; HEART LEFT VENTRICLE MASS; HEART MUSCLE FIBROSIS; HEART VENTRICLE REMODELING; HEMODYNAMICS; HUMAN; HYPERTENSION; MACROPHAGE; MORBIDITY; MORTALITY; MYOCARDITIS; NONHUMAN; NOTE; PATHOPHYSIOLOGY; PRIORITY JOURNAL; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM;

DIASTOLE; FIBROSIS; HEART DISEASES; HUMANS; HYPERTENSION; INFLAMMATION; RENIN-ANGIOTENSIN SYSTEM; SMAD3 PROTEIN; STROKE VOLUME; SYSTOLE;

EID: 77951499220     PISSN: 0194911X     EISSN: None     Source Type: Journal    
DOI: 10.1161/HYPERTENSIONAHA.110.150466     Document Type: Note

References (10)

1. Lee DS, Gona P, Vasan RS, Larson MG, Benjamin EJ, Wang TJ, Tu JV, Levy D. Relation of disease pathogenesis and risk factors to heart failure with preserved or reduced ejection fraction: insights from the framingham heart study of the national heart, lung, and blood institute. Circulation. 2009;119:3070-3077.
2. Diez J, Frohlich ED. A translational approach to hypertensive heart disease. Hypertension. 2010;55:1-8.
3. Klingbeil AU, Schneider M, Martus P, Messerli FH, Schmieder RE. A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. The Am J Med. 2003;115:41-46. (Pubitemid 36831120)
4. Tokuda K, Kai H, Kuwahara F, Yasukawa H, Tahara N, Kudo H, Takemiya K, Koga M, Yamamoto T, Imaizumi T. Pressure-independent effects of angiotensin II on hypertensive myocardial fibrosis. Hypertension. 2004;43:499-503. (Pubitemid 38174161)
5. Kuwahara F, Kai H, Tokuda K, Takeya M, Takeshita A, Egashira K, Imaizumi T. Hypertensive myocardial fibrosis and diastolic dysfunction: another model of inflammation? Hypertension. 2004;43:739-745. (Pubitemid 38405580)
6. Flanders KC. Smad3 as a mediator of the fibrotic response. Int J Exp Pathol. 2004;85:47-64.
7. Ashcroft GS, Yang X, Glick AB, Weinstein M, Letterio JL, Mizel DE, Anzano M, Greenwell-Wild T, Wahl SM, Deng C, Roberts AB. Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response. Nat Cell Biol. 1999;1:260-266. (Pubitemid 129495775)
8. Bujak M, Ren G, Kweon HJ, Dobaczewski M, Reddy A, Taffet G, Wang XF, Frangogiannis NG. Essential role of SMAD3 in infarct healing and in the pathogenesis of cardiac remodeling. Circulation. 2007;116: 2127-2138. (Pubitemid 350060350)
9. Divakaran V, Adrogue J, Ishiyama M, Entman ML, Haudek S, Sivasu-bramanian N, Mann DL. Adaptive and maladptive effects of SMAD3 signaling in the adult heart after hemodynamic pressure overloading. Circulation. 2009;2:633-642.
10. Huang XR, Chung ACK, Yang F, Yue W, Deng C, Lau CP, Tse HF, Lan HY. Smad3 mediates cardiac inflammation and fibrosis in angiotensin II-induced hypertensive cardiac remodeling. Hypertension. 2010;55: 1165-1171.