Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Marcin Bujak"'
Publikováno v:
Interventional cardiology clinics. 3(4)
Development of aortoiliac occlusive disease (AIOD) is associated with classic risk factors for atherosclerotic disease such as hyperlipidemia, hypertension, diabetes, or smoking. Risk factor modification, smoking cessation, and prevention of cardiova
Autor:
Erik Stilp, Jason Litsky, Stephanie M. Meller, Marcin Bujak, Nicolas Cal, Carlos Mena, John F. Setaro
Publikováno v:
Catheterization and Cardiovascular Interventions. 85:282-291
Percutaneous carotid artery stenting (CAS) has emerged as a less invasive alternative to carotid endarterectomy for the treatment of carotid atherosclerotic disease. The main risk of CAS is the occurrence of neuro-vascular complications; however, car
Autor:
Craig Gerard, Marcin Dobaczewski, Olga Frunza, Carlos Gonzalez-Quesada, Marcin Bujak, Nikolaos G. Frangogiannis, Amit Saxena, Bao Lu
Publikováno v:
Cardiovascular Research. 103:217-227
Aims The CXC chemokine CXCL10 is up-regulated in the infarcted myocardium and limits cardiac fibrosis by inhibiting growth factor-mediated fibroblast migration. CXCL10 signals by binding to its receptor CXCR3; however, recently CXCR3-independent CXCL
Autor:
Anilkumar K. Reddy, Panagiota Christia, Marcin Dobaczewski, Carlos Gonzalez-Quesada, Wei Chen, Marcin Bujak, Nikolaos G. Frangogiannis
Publikováno v:
Journal of Histochemistry & Cytochemistry. 61:555-570
Mouse models of myocardial infarction are essential tools for the study of cardiac injury, repair, and remodeling. Our current investigation establishes a systematic approach for quantitative evaluation of the inflammatory and reparative response, ca
Autor:
Na Li, Carlos Gonzalez-Quesada, Leonardo H. Mendoza, Marcin Dobaczewski, Marcin Bujak, Nikolaos G. Frangogiannis, Xaiao Fan Wang
Publikováno v:
Circulation Research. 107:418-428
Rationale: Cardiac fibroblasts are key effector cells in the pathogenesis of cardiac fibrosis. Transforming growth factor (TGF)-β/Smad3 signaling is activated in the border zone of healing infarcts and induces fibrotic remodeling of the infarcted ve
Autor:
Carlos Gonzalez-Quesada, Marcin Bujak, Nikolaos G. Frangogiannis, Ying Xia, Vikas Veeranna, Thorsten M Leucker, Andrew D. Luster, Andrew M. Tager, Marcin Dobaczewski, Pawel Zymek
Publikováno v:
Circulation Research. 105:973-983
Rationale: Interferon-γ-inducible protein (IP)-10/CXCL10, an angiostatic and antifibrotic chemokine with an important role in T-cell trafficking, is markedly induced in myocardial infarcts, and may regulate the reparative response. Objective: To stu
Autor:
Xia Ying, Peter Huebener, Tareq Abou-Khamis, Khaled Chatila, Sandra B. Haudek, Pawel Zymek, Marcin Bujak, Nikolaos G. Frangogiannis, Geeta D. Thakker
Publikováno v:
The Journal of Immunology. 180:2625-2633
Infarct healing is dependent on an inflammatory reaction that results in leukocyte infiltration and clearance of the wound from dead cells and matrix debris. However, optimal infarct healing requires timely activation of “stop signals” that suppr
Autor:
Xiao-Fan Wang, Marcin Dobaczewski, Marcin Bujak, Nikolaos G. Frangogiannis, Hyuk Jung Kweon, George E. Taffet, Anilkumar K. Reddy, Guofeng Ren
Publikováno v:
Circulation. 116:2127-2138
Background—Postinfarction cardiac repair is regulated through timely activation and repression of inflammatory pathways, followed by transition to fibrous tissue deposition and formation of a scar. The transforming growth factor-β/Smad3 pathway is
Autor:
Pawel Zymek, Marcin Bujak, Deuk Young Nah, Nikolaos G. Frangogiannis, Peter Huebener, Anna Koerting, Thorsten M Leucker, George E. Taffet, Guofeng Ren, Mark L. Entman
Publikováno v:
Cardiovascular Research. 74:313-322
Objective : Interleukin-10 (IL-10) exerts potent anti-inflammatory actions and modulates matrix metalloproteinase expression. We hypothesized that endogenous IL-10 may regulate infarct healing and left ventricular remodeling by promoting resolution o
Publikováno v:
Cardiovascular Research. 74:184-195
Transforming Growth Factor (TGF)-beta is markedly induced and rapidly activated in the infarcted myocardium. However, understanding of the exact role of TGF-beta signaling in the infarcted and remodeling heart has been hampered by the complex and unu