Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation.
<h4>Background</h4>Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could there...
Main Authors: | Christina Pachel, Denise Mathes, Barbara Bayer, Charlotte Dienesch, Gaby Wangorsch, Wolfram Heitzmann, Isabell Lang, Hossein Ardehali, Georg Ertl, Thomas Dandekar, Harald Wajant, Stefan Frantz |
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Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2013-01-01
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Series: | PLoS ONE |
Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24244389/pdf/?tool=EBI |
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