TREM-1 Mediates Inflammatory Injury and Cardiac Remodeling Following Myocardial Infarction.
Fiche publication
Date publication
mai 2015
Journal
Circulation research
Auteurs
Membres identifiés du Cancéropôle Est :
Pr MARIE Pierre-Yves
Tous les auteurs :
Boufenzer A, Lemarié J, Simon T, Derive M, Bouazza Y, Tran N, Maskali F, Groubatch F, Bonnin P, Bastien C, Bruneval P, Marie PY, Cohen R, Danchin N, Silvestre JS, Ait-Oufella H, Gibot S
Lien Pubmed
Résumé
Optimal outcome after myocardial infarction (MI) depends on a coordinated healing response in which both debris removal and repair of the myocardial extracellular matrix play a major role. However, adverse remodeling and excessive inflammation can promote heart failure, positioning leucocytes as central protagonists and potential therapeutic targets in tissue repair and wound healing after MI.
Mots clés
Acute Disease, Amino Acid Sequence, Animals, Blotting, Western, Coronary Disease, blood, Gene Expression, Humans, Inflammation, genetics, Leukocytes, metabolism, Male, Membrane Glycoproteins, antagonists & inhibitors, Mice, Inbred C57BL, Mice, Knockout, Myocardial Infarction, genetics, Peptides, pharmacology, Rats, Wistar, Receptors, Immunologic, antagonists & inhibitors, Reverse Transcriptase Polymerase Chain Reaction, Survival Analysis, Ventricular Function, Left, drug effects, Ventricular Remodeling, drug effects
Référence
Circ. Res.. 2015 May;116(11):1772-82