Using the laws of thermodynamics to understand how matrix metalloproteinases coordinate the myocardial response to injury
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[1] P. Libby,et al. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. , 2000, The Journal of clinical investigation.
[2] P. Lemarchand,et al. Intramyocardial Delivery of Mesenchymal Stem Cell-Seeded Hydrogel Preserves Cardiac Function and Attenuates Ventricular Remodeling after Myocardial Infarction , 2012, PloS one.
[3] Nguyen T. Nguyen,et al. Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. , 2012, Journal of molecular and cellular cardiology.
[4] N. Chattipakorn,et al. Matrix metalloproteinases and myocardial infarction. , 2007, The Canadian journal of cardiology.
[5] Trevi A. Ramirez,et al. Aliskiren and valsartan mediate left ventricular remodeling post-myocardial infarction in mice through MMP-9 effects. , 2014, Journal of molecular and cellular cardiology.
[6] Andrew P. Voorhees,et al. Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac Dysfunction and Rupture After Myocardial Infarction in Mice by Inhibiting M2 Macrophage Activation , 2012, Circulation research.
[7] Yu-Fang Jin,et al. Matrix Metalloproteinase-28 Deletion Amplifies Inflammatory and Extracellular Matrix Responses to Cardiac Aging , 2011, Microscopy and Microanalysis.
[8] C. Kramer,et al. Mechanisms of Post-Infarct Left Ventricular Remodeling. , 2007, Drug discovery today. Disease mechanisms.
[9] S. Takai,et al. Molecular mechanism of imidapril for cardiovascular protection via inhibition of MMP-9. , 2007, Journal of molecular and cellular cardiology.
[10] N. Frangogiannis,et al. The inflammatory response in myocardial injury, repair, and remodelling , 2014, Nature Reviews Cardiology.
[11] Michael E. Hall,et al. Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction. , 2014, American journal of physiology. Heart and circulatory physiology.
[12] Zhonglin Xie,et al. Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin , 2001, Circulation research.
[13] Wei Wang,et al. Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction. , 2010, American journal of physiology. Heart and circulatory physiology.
[14] M. Czubryt. Common threads in cardiac fibrosis, infarct scar formation, and wound healing , 2012, Fibrogenesis & tissue repair.
[15] G. Gabbiani,et al. Presence of modified fibroblasts in granulation tissue and their possible role in wound contraction , 1971, Experientia.
[16] G. Lamas,et al. Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial. , 1997, Circulation.
[17] M. Lindsey,et al. Translating Koch's postulates to identify matrix metalloproteinase roles in postmyocardial infarction remodeling: cardiac metalloproteinase actions (CarMA) postulates. , 2014, Circulation research.
[18] M. Lindsey,et al. Myocardial matrix metalloproteinase-2: inside out and upside down. , 2014, Journal of molecular and cellular cardiology.
[19] M. Pfeffer,et al. Ventricular Remodeling After Myocardial Infarction: Experimental Observations and Clinical Implications , 1990, Circulation.
[20] M. Lindsey,et al. Matrix metalloproteinase (MMP)-9: a proximal biomarker for cardiac remodeling and a distal biomarker for inflammation. , 2013, Pharmacology & therapeutics.
[21] R. Vracko,et al. Contractile cells in rat myocardial scar tissue. , 1991, Laboratory investigation; a journal of technical methods and pathology.
[22] P. Libby,et al. Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental myocardial infarction in mice. , 1999, Circulation.
[23] S. Takai,et al. Pharmacological implications of MMP-9 inhibition by ACE inhibitors. , 2009, Current medicinal chemistry.
[24] Yu-Fang Jin,et al. Multi-Analyte Profiling Reveals Matrix Metalloproteinase-9 and Monocyte Chemotactic Protein-1 as Plasma Biomarkers of Cardiac Aging , 2011, Circulation. Cardiovascular genetics.
[25] S. Takai,et al. Prediction of interaction mode between a typical ACE inhibitor and MMP-9 active site. , 2007, Biochemical and biophysical research communications.
[26] Trevi A. Ramirez,et al. Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice. , 2012, Cardiovascular research.
[27] Richard T. Lee,et al. Selective Matrix Metalloproteinase Inhibition Reduces Left Ventricular Remodeling but Does Not Inhibit Angiogenesis After Myocardial Infarction , 2002, Circulation.
[28] M. Zile,et al. Myocardial Infarct Expansion and Matrix Metalloproteinase Inhibition , 2003, Circulation.
[29] Y. Okada,et al. Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice. , 2005, The Journal of clinical investigation.
[30] S. Redwood,et al. Late intervention after anterior myocardial infarction: effects on left ventricular size, function, quality of life, and exercise tolerance: results of the Open Artery Trial (TOAT Study). , 2002, Journal of the American College of Cardiology.
[31] M. Lindsey,et al. Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence. , 2015, Cardiovascular research.
[32] R. Khokha,et al. Mice with Tissue Inhibitor of Metalloproteinases 4 (Timp4) Deletion Succumb to Induced Myocardial Infarction but Not to Cardiac Pressure Overload* , 2010, The Journal of Biological Chemistry.
[33] G. Lamas,et al. Ventricular remodeling after myocardial infarction. , 1993, Advances in experimental medicine and biology.
[34] Stephane Heymans,et al. Relevance of matrix metalloproteinases and their inhibitors after myocardial infarction: a temporal and spatial window. , 2006, Cardiovascular research.
[35] Richard T. Lee,et al. Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction. , 2006, American journal of physiology. Heart and circulatory physiology.
[36] E. Creemers,et al. Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice. , 2003, American journal of physiology. Heart and circulatory physiology.
[37] A. Cohen-Solal,et al. [Ventricular "remodeling" after myocardial infarction]. , 1991, Archives des maladies du coeur et des vaisseaux.
[38] T. Abraham,et al. TIMP2 Deficiency Accelerates Adverse Post–Myocardial Infarction Remodeling Because of Enhanced MT1-MMP Activity Despite Lack of MMP2 Activation , 2010, Circulation research.
[39] M. Lindsey,et al. Citrate synthase is a novel in vivo matrix metalloproteinase-9 substrate that regulates mitochondrial function in the postmyocardial infarction left ventricle. , 2014, Antioxidants & redox signaling.
[40] M. Lindsey,et al. Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution. , 2015, International journal of cardiology.
[41] A. Luttun,et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure , 1999, Nature Medicine.
[42] Christine N. Koval,et al. Cardiac Restricted Overexpression of Membrane Type-1 Matrix Metalloproteinase Causes Adverse Myocardial Remodeling following Myocardial Infarction* , 2010, The Journal of Biological Chemistry.
[43] F. Eberli,et al. ET(A)-receptor blockade prevents matrix metalloproteinase activation late postmyocardial infarction in the rat. , 2001, American journal of physiology. Heart and circulatory physiology.
[44] M. Zile,et al. Accelerated LV remodeling after myocardial infarction in TIMP-1-deficient mice: effects of exogenous MMP inhibition. , 2005, American journal of physiology. Heart and circulatory physiology.
[45] M. Daemen,et al. Collagen remodeling after myocardial infarction in the rat heart. , 1995, The American journal of pathology.
[46] F. Spinale,et al. Selective Targeting and Timing of Matrix Metalloproteinase Inhibition in Post-Myocardial Infarction Remodeling , 2003, Circulation.
[47] N. Frangogiannis,et al. Regulation of the inflammatory response in cardiac repair. , 2012, Circulation research.