Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction.
By A. Ducharme, S. Frantz, M. Aikawa, E. Rabkin, M. Lindsey, Luis E. Rohde, F. Schoen, R. Kelly, Zena Werb, Peter Libby and 1 more. Journal of Clinical Investigation, 2000
842 citations recorded by the source corpus.
Subfields: Cancer Research, Cardiology and Cardiovascular Medicine, Oncology
View Paper: https://www.semanticscholar.org/paper/78e258f57f266f48b58dba76a55ab8552b483d44
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In Cancer Research
- Gillian Murphy
- Hideaki Nagase
- Zena Werb
- Francis G. Spinale
- Z. Kassiri
- A. Takawale
- Asish K. Ghosh
- Douglas E. Vaughan
In Cardiology and Cardiovascular Medicine
In Oncology
- Gillian Murphy
- Hideaki Nagase
- Zena Werb
- Francis G. Spinale
- Z. Kassiri
- A. Takawale
- Asish K. Ghosh
- Douglas E. Vaughan
Citations in the corpus
- Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. (2007, methodology): “Accordingly, it would follow that this specific MMP was the focus of targeted gene deletion in murine constructs (98, 161, 237).”
- Evidence from a genetic fate-mapping study that stem cells refresh adult mammalian cardiomyocytes after injury (2007, methodology): “Myocardial infarction was produced by permanent ligation of the left coronary artery ∼3 mm below the left atrial appendix, as describe”
- Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease (2012, background): “MMP9 deletion provided partial protection against post-MI rupture [138], while reducing LV dilation and dysfunction [139].”
- PAI-1 in Tissue Fibrosis (2012, background): “The proteolytic activity of MMP2 and MMP9 are known to play a significant role in the initiation and progression of cardiac fibrosis (Ducharme et al., 2000; Matsusaka et al., 2006).”
- Cellular and molecular mechanisms in kidney fibrosis. (2014, positive): “Gene mutation studies do not fully support this as the major mechanism, since such targeted mutations indicate many MMPs, including MMP9, cleave and activate a small number of discrete protein targets rather than significantly degrade matrix (84, 85).”
- Gelatinase B functions as regulator and effector in leukocyte biology (2001, neutral): “Altered, post-myocardial infarction cardiac remodeling [ 46 ]”
- Progress in matrix metalloproteinase research. (2008, background): “…(2005b) Mmp9 Reduction neointima formation on vascular injury Johnson and Galis (2004) Protection from cardiac rupture post-myocardial infarction Ducharme et al. (2000) Mmp11 Accelerated neointima formation on vascular injury Lijnen et al. (1999b) Timp1 Accelerated neointima formation on…”
- How matrix metalloproteinases regulate cell behavior. (2001, background): “…to experimental aortic aneurysms (Pyo et al. 2000) Prolonged contact dermatitis (Wang et al. 1999) Protection from ventricular enlargement after infarction (Ducharme et al. 2000) Protection from cardiac rupture following infarction (Heymans et al. 1999) Diminished motor defects following brain…”
- Matrix metalloproteinase-9: Many shades of function in cardiovascular disease. (2013, background): “In MI, MMP-9-deficient mice showed reduced rupture rate and attenuated ventricular dilation, which was associated with reduced macrophage infiltration (23).”