Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Juozas A. Zavadzkas"'
Autor:
Laurel Black, Evan C. Meyer, Risha K Patel, Robert E. Stroud, William T Rivers, J. Marshall Oelsen, Rupak Mukherjee, Francis G. Spinale, Richard A McKinney, Juozas A. Zavadzkas
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 301:H1656-H1666
The membrane type 1 matrix metalloproteinase (MT1-MMP) is increased in left ventricular (LV) failure. However, the direct effects of altered MT1-MMP levels on survival, LV function, and geometry following myocardial infarction (MI) and the proteolyti
Autor:
John S. Ikonomidis, Robert E. Stroud, Jeffrey A. Jones, Juozas A. Zavadzkas, Eileen I. Chang, Christine N. Koval, Francis G. Spinale, Nina J Sheats
Publikováno v:
The Journal of Thoracic and Cardiovascular Surgery. 140(3):653-659
Objective Thoracic aortic aneurysms result from dysregulated remodeling of the vascular extracellular matrix, which may occur as a result of altered resident cellular function. The present study tested the hypothesis that aortic fibroblasts undergo a
Autor:
Jeffrey A. Jones, Jean Marie Ruddy, John S. Ikonomidis, Theresa A. Brinsa, Shenikqua Bouges, Francis G. Spinale, Rupak Mukherjee, Robert E. Stroud, Juozas A. Zavadzkas
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 299:H114-H124
Thoracic aortic aneurysms (TAAs) develop as a result of dysregulated extracellular matrix remodeling mediated by several matrix metalloproteinases (MMPs). Membrane type-1 MMP (MT1-MMP) is the prototypical member of a unique family of membrane-bound M
Autor:
Juozas A. Zavadzkas, Julie E. McLean, Robert G. Matthews, Robert E. Stroud, Shenikqua Bouges, Rupak Mukherjee, Christine N. Koval, William T Rivers, Eileen I. Chang, Francis G. Spinale
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 299:H217-H224
Increased matrix metalloproteinase (MMP) abundance occurs with adverse left ventricular (LV) remodeling in a number of cardiac disease states, including those induced by long-standing arrhythmias. However, whether regionally contained aberrant electr
Autor:
Sundaravadivel Balasubramanian, Francis G. Spinale, Dhandapani Kuppuswamy, Rupak Mukherjee, Santhosh K. Mani, William T Rivers, Michael R. Zile, Juozas A. Zavadzkas, Laura B Jeffords
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 297:H1744-H1751
Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(
Autor:
Allyson M. Leone, Stuart M. Saunders, Robert E. Stroud, G. Patricia Escobar, Laura B Jeffords, Christy Beck, Francis G. Spinale, Shenikqua Bouges, Rupak Mukherjee, Juozas A. Zavadzkas
Publikováno v:
Circulation: Heart Failure. 2:351-360
Background— The direct consequences of a persistently increased myocardial expression of the unique matrix metalloproteinase (MMP) membrane type-1 (MT1-MMP) on myocardial remodeling remained unexplored. Methods and Results— Cardiac-restricted MT1
Autor:
Michel J. Sabbagh, Francis G. Spinale, William T Rivers, J Michael Looper, Rachael L Ford, Robert E. Stroud, Scott Reeves, Juozas A. Zavadzkas, Matthew D. McEvoy, Christine N. Koval
Publikováno v:
Journal of Cardiovascular Pharmacology. 52:355-362
Aprotinin is a serine protease inhibitor with diverse biological effects; until recently, it was utilized in the context of ischemia/reperfusion (I/R). It has been hypothesized that a signaling pathway modulated by aprotinin in the context of I/R is
Autor:
Francis G. Spinale, Laura B Jeffords, Anne M. Deschamps, Rebecca L. Murphy, Nina J Sheats, Stuart M. Saunders, Robert E. Stroud, Christine N. Koval, Julie E. McLean, Juozas A. Zavadzkas
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 294:H875-H883
The matrix metalloproteinases (MMPs), in particular, membrane type 1 MMP (MT1-MMP), are increased in the context of myocardial ischemia and reperfusion (I/R) and likely contribute to myocardial dysfunction. One potential upstream induction mechanism
Autor:
Francis G. Spinale, Paul J. McDermott, Risha K Patel, Juozas A. Zavadzkas, Jeffrey R. Jones, Robert E. Stroud, Shenikqua Bouges, Rupak Mukherjee
Rationale: Myocardial infarction (MI) causes an imbalance between matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases (TIMPs) and is associated with adverse left ventricular (LV) remodeling. A uniform reduction in TIMP-4 post
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8f1e0101a73b29cb04441333ff2991f2
https://europepmc.org/articles/PMC4040980/
https://europepmc.org/articles/PMC4040980/
Publikováno v:
The American Surgeon. 76:117-119