Dr Frangogiannis’ research explores the mechanisms of cardiac injury and repair. His laboratory has identified key molecular signals responsible for orchestrating the healing response in myocardial infarction. Research has focused on four main directions:
a) The role of chemokine-mediated pathways in cardiac injury and repair. Current research studies the significance of specific chemokine/chemokine receptor interactions in recruitment of monocyte and lymphocyte subsets with anti-inflammatory properties.
b) Signals involved in resolution of the inflammatory reaction and in containment of the fibrotic response following infarction. Dr Frangogiannis’ laboratory has identified endogenous molecular pathways preventing excessive inflammation and uncontrolled fibrosis following cardiac injury.
c) The role of the dynamic alterations in the composition of the extracellular matrix network in modulating inflammatory pathways and cellular behavior in the injured and remodeling heart.
d) The mechanisms involved in the pathogenesis of cardiac fibrosis in the cardiomyopathy associated with diabetes and obesity.
The goal of the Frangogiannis laboratory is to identify therapeutic targets for attenuation of adverse remodeling following cardiac injury, thus preventing the development of heart failure.
Selected recent publications:
M Bujak, G Ren, HJ Kweon, M Dobaczewski, A Reddy, G Taffet, XF Wang, and NG Frangogiannis. Essential Role of Smad3 in Infarct Healing and in the Pathogenesis of Cardiac Remodeling. Circulation 2007; 116:2127-38.
P Huebener, T Abou-Khamis, P Zymek, M Bujak, Ying X, K Chatila, S Haudek, G Thakker, and NG Frangogiannis, CD44 is critically involved in infarct healing by regulating the inflammatory and fibrotic response. J Immunol 2008; 180:2625-33.
M Bujak, HJ Kweon, K Chatila, N Li, G Taffet and NG Frangogiannis. Aging-related defects are associated with adverse cardiac remodeling in a mouse model of reperfused myocardial infarction. J Am Coll Cardiol 2008; 51:1384-92.
M Bujak, M Dobaczewski, K Chatila, L Mendoza, N Li, A Reddy, and NG Frangogiannis. Interleukin-1 type (IL-1RI) signaling critically regulates infarct healing and cardiac remodeling. Am J Pathol 2008; 173:57-67.
M Bujak, M Dobaczewski, C Gonzalez-Quesada, Y Xia, T Leucker, P Zymek, V Veeranna, A Tager, A Luster, and NG Frangogiannis. Induction of the CXC Chemokine Interferon-g-Inducible Protein (IP)-10 Regulates the Reparative Response Following Myocardial Infarction. Circ Res 2009; 105:973-83.
M Dobaczewski, Y Xia, M Bujak, C Gonzalez-Quesada, and NG Frangogiannis. CCR5 signaling suppresses inflammation and reduces adverse remodeling following myocardial infarction mediating recruitment of regulatory T cells. Am J Pathol 2010; 176: 2177-87.
M Dobaczewski, M Bujak, N Li, C Gonzalez-Quesada; LH Mendoza, XF Wang, and NG Frangogiannis. Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction. Circ Res 2010; 107 (3): 418-28.
Y Xia, M Dobaczewski, C Gonzalez-Quesada, W Chen, A Biernacka, N Li, D Lee and NG Frangogiannis. Endogenous Thrombospondin-1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolism. Hypertension 2011; 58: 902-911.
NG Frangogiannis. Regulation of the inflammatory response in cardiac repair. Circ Res 2012: 110: 159-173.
NG Frangogiannis. Matricellular proteins in cardiac adaptation and disease. Physiol Rev 2012; 92:635-688.
W Chen, A Saxena, N Li, J Sun, DW Lee, Q Tian, M Dobaczewski and NG Frangogiannis. Endogenous IRAK-M attenuates post-infarction remodeling through effects on macrophages and fibroblasts. Arterioscl Thromb Vasc Biol 2012; 32:2598-608.
A Saxena, W Chen, Y Su, V Rai, OU Uche, N Li, and NG Frangogiannis. IL-1 induces proinflammatory leukocyte infiltration and regulates fibroblast phenotype in the infarcted myocardium. J Immunol 2013; 191(9):4838-48.
C Gonzalez-Quesada, M Cavalera, A Biernacka, P Kong, DW Lee, A Saxena, O Frunza, M Dobaczewski, AV Shinde, and NG Frangogiannis. Thrombospondin-1 induction in the diabetic myocardium stabilizes the cardiac matrix while promoting vascular rarefaction through angiopoietin-2 upregulation. Circ Res 2013; 113(12):1331-44.
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