TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
about
HMGB1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and miR-206-mediated inhibition of TIMP-3Injectable and bioresponsive hydrogels for on-demand matrix metalloproteinase inhibitionThe tissue inhibitors of metalloproteinases (TIMPs): an ancient family with structural and functional diversityEarly activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction.Sulfated glycosaminoglycans control the extracellular trafficking and the activity of the metalloprotease inhibitor TIMP-3.Integrative computational and experimental approaches to establish a post-myocardial infarction knowledge map.MT1-MMP-dependent remodeling of cardiac extracellular matrix structure and function following myocardial infarctionTIMP3 interplays with apelin to regulate cardiovascular metabolism in hypercholesterolemic mice.Extracellular matrix turnover and signaling during cardiac remodeling following MI: causes and consequences.Ventricular remodeling and function: insights using murine echocardiography.Matrix metalloproteinase therapy in heart failure.Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction.Tissue inhibitor of metalloproteinases (TIMPs) in heart failure.Differential effects of dexamethasone and rosiglitazone in a sephadex-induced model of lung inflammation in rats: possible role of tissue inhibitor of metalloproteinase-3Low tissue inhibitor of metalloproteinases 3 and high matrix metalloproteinase 14 levels defines a subpopulation of highly invasive foam-cell macrophages.Myocardial overexpression of TIMP3 after myocardial infarction exerts beneficial effects by promoting angiogenesis and suppressing early proteolysis.Cardiac tissue inhibitor of matrix metalloprotease 4 dictates cardiomyocyte contractility and differentiation of embryonic stem cells into cardiomyocytes: Road to therapy.Mice with tissue inhibitor of metalloproteinases 4 (Timp4) deletion succumb to induced myocardial infarction but not to cardiac pressure overload.Tissue inhibitor of metalloproteinase-2 gene delivery ameliorates postinfarction cardiac remodeling.Dissecting the Role of the Extracellular Matrix in Heart Disease: Lessons from the Drosophila Genetic Model.Inhibiting matrix metalloproteinase by cell-based timp-3 gene transfer effectively treats acute and chronic ischemic cardiomyopathy.Densification of Type I Collagen Matrices as a Model for Cardiac Fibrosis.A single injection of protein-loaded coacervate-gel significantly improves cardiac function post infarction.
P2860
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P2860
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh
2007年學術文章
@zh-hant
name
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@en
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@nl
type
label
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@en
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@nl
prefLabel
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@en
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.
@nl
P2093
P50
P1476
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction
@en
P2093
Massimo Cimini
Ming-Li Huang
Richard D Weisel
Shafie Fazel
Svetlana Altamentova
P304
P356
10.1016/J.YJMCC.2007.09.003
P577
2007-09-14T00:00:00Z