Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.
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Cellular and molecular mechanisms of fibrosisAlways cleave up your mess: targeting collagen degradation to treat tissue fibrosisBiochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9): the next decadeGlobal gene expression profiling in PAI-1 knockout murine heart and kidney: molecular basis of cardiac-selective fibrosisLipopolysaccharide upregulates uPA, MMP-2 and MMP-9 via ERK1/2 signaling in H9c2 cardiomyoblast cellsSalvianolic acid B functioned as a competitive inhibitor of matrix metalloproteinase-9 and efficiently prevented cardiac remodelingAdiponectin deficiency, diastolic dysfunction, and diastolic heart failure.Transcriptional changes in bone marrow stromal cells of patients with heart failure.Interleukin-18 induces EMMPRIN expression in primary cardiomyocytes via JNK/Sp1 signaling and MMP-9 in part via EMMPRIN and through AP-1 and NF-kappaB activationMatrix metalloproteinases and protein tyrosine kinases: potential novel targets in acute lung injury and ARDSUrokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophagesUrokinase and its receptors in chronic kidney disease.Matrix metalloproteinase 3 is a mediator of pulmonary fibrosis.Decreased metalloprotease 9 induction, cardiac fibrosis, and higher autophagy after pressure overload in mice lacking the transcriptional regulator p8.Fibulin-5 binds urokinase-type plasminogen activator and mediates urokinase-stimulated β1-integrin-dependent cell migration.Correlation between growth differentiation factor-15 and collagen metabolism indicators in patients with myocardial infarction and heart failure.Improvement of left ventricular remodeling after myocardial infarction with eight weeks L-thyroxine treatment in ratsECM remodeling in hypertensive heart disease.Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases.Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology.Cardiac tissue factor: roles in physiology and fibrosis.Extracellular matrix profiles in the progression to heart failure. European Young Physiologists Symposium Keynote Lecture-Bratislava 2007.Matrix metalloproteinase-9: Many shades of function in cardiovascular disease.Matrix metalloproteinases and their tissue inhibitors in cardiac amyloidosis: relationship to structural, functional myocardial changes and to light chain amyloid deposition.Overexpression of SerpinE2/protease nexin-1 Contribute to Pathological Cardiac Fibrosis via increasing Collagen Deposition.Ventricular remodeling and function: insights using murine echocardiography.Role of the urokinase plasminogen activator receptor in mediating impaired efferocytosis of anti-SSA/Ro-bound apoptotic cardiocytes: Implications in the pathogenesis of congenital heart block.Emerging concepts in cardiac matrix biology.A Clinical Perspective of Anti-Fibrotic Therapies for Cardiovascular Disease.PAI-1 in tissue fibrosis.Mitochondrial mitophagic mechanisms of myocardial matrix metabolism and remodelling.Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease.Role of inflammation in the pathogenesis of heart failure with preserved ejection fraction and its potential as a therapeutic target.The importance of matrix metalloproteinase-3 in respiratory disorders.Gene expression profiling of human mesenchymal stem cells for identification of novel markers in early- and late-stage cell culture.Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness.Unmet Needs in the Pathogenesis and Treatment of Cardiovascular Comorbidities in Chronic Inflammatory Diseases.ZAK induces MMP-2 activity via JNK/p38 signals and reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells.The oxygen free radicals control MMP-9 and transcription factors expression in the spontaneously hypertensive rat.Tissue inhibitor of metalloproteinase-1 and -3 improves cardiac function in an ischemic cardiomyopathy model rat.
P2860
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P2860
Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Loss or inhibition of uPA or M ...... ute pressure overload in mice.
@en
type
label
Loss or inhibition of uPA or M ...... ute pressure overload in mice.
@en
prefLabel
Loss or inhibition of uPA or M ...... ute pressure overload in mice.
@en
P2093
P2860
P1476
Loss or inhibition of uPA or M ...... ute pressure overload in mice.
@en
P2093
Andrew Baker
Bjorn Vanwetswinkel
Desire Collen
Florea Lupu
Jean-Marc Herbert
Lieve Moons
Stephane Heymans
Sven Terclavers
P2860
P356
10.1016/S0002-9440(10)62228-6
P407
P577
2005-01-01T00:00:00Z