Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. (Q36319909)

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English	Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction.	scientific article

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10 February 2020

Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction (English)

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Lisandra E de Castro Brás

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Merry L. Lindsey

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author name string

Rogelio Zamilpa

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Jessica Ibarra

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Trevi A Ramirez

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Nguyen Nguyen

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Ganesh V Halade

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Jianhua Zhang

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Qiuxia Dai

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Tariq Dayah

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Ying Ann Chiao

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Wesley Lowell

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Seema S Ahuja

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Jeanine D'Armiento

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Yu-Fang Jin

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publication date

3 August 2012

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10 February 2020

Journal of Molecular and Cellular Cardiology

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599-608

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5

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10 February 2020

CC chemokine receptor 5 deletion impairs macrophage activation and induces adverse remodeling following myocardial infarction.

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30 September 2017

Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction.

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30 September 2017

Monocytes: protagonists of infarct inflammation and repair after myocardial infarction

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30 September 2017

Altered lymphocyte trafficking and diminished airway reactivity in transgenic mice expressing human MMP-9 in a mouse model of asthma

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Identification of splenic reservoir monocytes and their deployment to inflammatory sites

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P43/pro-EMAPII: a potential biomarker for discriminating traumatic versus ischemic brain injury

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Macrophage diversity in renal injury and repair.

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30 September 2017

Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice

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30 September 2017

Macrophage roles following myocardial infarction

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30 September 2017

Periostin is essential for cardiac healing after acute myocardial infarction

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30 September 2017

Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study

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30 September 2017

Potential role for antiangiogenic proteins in the myocardial infarction repair process

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30 September 2017

Endothelial monocyte activating polypeptide II (EMAP II) enhances the effect of TNF on tumor-associated vasculature

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30 September 2017

Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction

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30 September 2017

Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction.

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29 June 2018

Accumulation of fibronectin in the heart after myocardial infarction: a putative stimulator of adhesion and proliferation of adipose-derived stem cells

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29 June 2018

Macrophage depletion impairs wound healing and increases left ventricular remodeling after myocardial injury in mice

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Identification of protease-sensitive sites in Human Endothelial-Monocyte Activating Polypeptide II protein

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Collagen remodeling after myocardial infarction in the rat heart

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29 June 2018

Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice.

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Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair.

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22 September 2018

Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction.

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22 September 2018

Relations of plasma matrix metalloproteinase-9 to clinical cardiovascular risk factors and echocardiographic left ventricular measures: the Framingham Heart Study.

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22 September 2018

Temporal changes in matrix metalloproteinase expression and inflammatory response associated with cardiac rupture after myocardial infarction in mice

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22 September 2018

Overexpression of MMP9 in macrophages attenuates pulmonary fibrosis induced by bleomycin

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Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure

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Increased Expression of Fibronectin Isoforms After Myocardial Infarction in Rats

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Tenascin and fibronectin expression in healing human myocardial scars

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TIMP2 deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activation

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10.1016/J.YJMCC.2012.07.017

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10 February 2020

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10 February 2020

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