Transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis. (Q47909549)

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scientific article published on 23 December 2016

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English	Transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis.	scientific article published on 23 December 2016

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1 April 2020

Transgenic overexpression of macrophage matrix metalloproteinase-9 exacerbates age-related cardiac hypertrophy, vessel rarefaction, inflammation, and fibrosis (English)

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Merry L. Lindsey

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Andriy Yabluchanskiy

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Hiroe Toba

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Presley L Cannon

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Rugmani Padmanabhan Iyer

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Jeanine D'Armiento

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23 December 2016

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American Journal of Physiology Heart and Circulatory Physiology

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312

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H375-H383

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1 April 2020

Increased ADAMTS1 mediates SPARC-dependent collagen deposition in the aging myocardium.

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Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization.

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Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.

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Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice

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

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Multi-analyte profiling reveals matrix metalloproteinase-9 and monocyte chemotactic protein-1 as plasma biomarkers of cardiac aging.

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Age-dependent changes in myocardial matrix metalloproteinase/tissue inhibitor of metalloproteinase profiles and fibroblast function

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Overexpression of MMP9 in macrophages attenuates pulmonary fibrosis induced by bleomycin

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Identifiers

10.1152/AJPHEART.00633.2016

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Europe PubMed Central

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1 April 2020

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1 April 2020

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1 April 2020

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