IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction. - Wikidata - wikimedia - TriplyDB

IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction.

IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction.

http://www.wikidata.org/entity/Q37040630

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Multifunctional Role of Chymase in Acute and Chronic Tissue Injury and Remodeling.Highly Selective Cleavage of Cytokines and Chemokines by the Human Mast Cell Chymase and Neutrophil Cathepsin G.Orphan receptor GPR37L1 contributes to the sexual dimorphism of central cardiovascular control.Simultaneous Delivery of Wharton's Jelly Mesenchymal Stem Cells and Insulin-Like Growth Factor-1 in Acute Myocardial Infarction.Chick Embryo: A Preclinical Model for Understanding Ischemia-Reperfusion Mechanism Mouse Mast Cell Protease 4 Deletion Protects Heart Function and Survival After Permanent Myocardial Infarction

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IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction.

http://www.wikidata.org/entity/Q37040630

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 06 June 2016

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

IGF-1 degradation by mouse mas ...... after a myocardial infarction.

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IGF-1 degradation by mouse mas ...... after a myocardial infarction.

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type

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IGF-1 degradation by mouse mas ...... after a myocardial infarction.

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IGF-1 degradation by mouse mas ...... after a myocardial infarction.

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prefLabel

IGF-1 degradation by mouse mas ...... after a myocardial infarction.

@en

IGF-1 degradation by mouse mas ...... after a myocardial infarction.

@nl

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PNAS.1603127113

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Proceedings of the National Academy of Sciences of the United States of America

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IGF-1 degradation by mouse mas ...... after a myocardial infarction.

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Ahsan Husain

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David J Lefer

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Gunnar Pejler

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Hussain Naib

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John W Calvert

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Jonathan P Lambert

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Lin Tan

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Madiha Zaidi

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Magnus Abrink

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Maria D Berce

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P2860

Identification of a highly specific chymase as the major angiotensin II-forming enzyme in the human heart

Rapid conversion of angiotensin I to angiotensin II by neutrophil and mast cell proteinases

The chymase, mouse mast cell protease 4, constitutes the major chymotrypsin-like activity in peritoneum and ear tissue. A role for mouse mast cell protease 4 in thrombin regulation and fibronectin turnover

A key role for mast cell chymase in the activation of pro-matrix metalloprotease-9 and pro-matrix metalloprotease-2.

The extended cleavage specificity of the rodent beta-chymases rMCP-1 and mMCP-4 reveal major functional similarities to the human mast cell chymase.

Mast cell chymase limits the cardiac efficacy of Ang I-converting enzyme inhibitor therapy in rodents

A proliferative burst during preadolescence establishes the final cardiomyocyte number.

Mouse mast cell protease-4 deteriorates renal function by contributing to inflammation and fibrosis in immune complex-mediated glomerulonephritis.

Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators.

Local myocardial insulin-like growth factor 1 (IGF-1) delivery with biotinylated peptide nanofibers improves cell therapy for myocardial infarction.

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6949-6954

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10.1073/PNAS.1603127113

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