title: Targeting danger-associated molecular patterns after myocardial infarction.
abstract: BACKGROUND
  Myocardial infarction (MI) provokes an intense inflammatory response that can lead to left ventricular adverse remodeling and heart failure (HF). The prognosis of HF patients is poor and related to a decreased quality of life and considerable health care costs. Hence, targeting the early inflammatory response after MI provides an interesting target to attenuate left ventricular remodeling and prevent HF.
  
  
  METHODS
  In the current review, we discuss the theory that our immune system does not distinguish between self and non-self, but rather senses danger. So-called danger-associated molecular patterns (DAMPs) serve as ligands for pattern recognition receptors (PRRs), which act as signal transduction molecules to induce a pro-inflammatory state. Many different DAMPs and PRRs have been identified recently. Here, we provide a concise overview of their interactions as well as their role in the inflammatory response after MI.
  
  
  CONCLUSIONS
  Interference with Toll-like receptor (TLR) 2, TLR4 and NLRP3-inflammasome signaling has consistently shown to reduce infarct size and preserve cardiac function post-MI in experimental animal models. Since clinically applicable inhibitors have been developed for these pathways, the path has been cleared to assess whether these promising results can be translated into the human situation.
authors.affiliation: a 1 University Medical Center Utrecht, Experimental Cardiology Laboratory , Utrecht, The Netherlands ; g.p.j.vanhout@umcutrecht.nl.
authors.forename: Gerardus P J
authors.initials: GP
authors.lastname: van Hout
authors.affiliation: a 1 University Medical Center Utrecht, Experimental Cardiology Laboratory , Utrecht, The Netherlands ; g.p.j.vanhout@umcutrecht.nl.
authors.forename: Fatih
authors.initials: F
authors.lastname: Arslan
authors.affiliation: a 1 University Medical Center Utrecht, Experimental Cardiology Laboratory , Utrecht, The Netherlands ; g.p.j.vanhout@umcutrecht.nl.|b 2 University Medical Center Utrecht, Department of Clinical Chemistry and Hematology , Utrecht, The Netherlands.
authors.forename: Gerard
authors.initials: G
authors.lastname: Pasterkamp
authors.affiliation: a 1 University Medical Center Utrecht, Experimental Cardiology Laboratory , Utrecht, The Netherlands ; g.p.j.vanhout@umcutrecht.nl.|b 2 University Medical Center Utrecht, Department of Clinical Chemistry and Hematology , Utrecht, The Netherlands.
authors.forename: Imo E
authors.initials: IE
authors.lastname: Hoefer
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015195:Drug Design; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology; D058990:Molecular Targeted Therapy; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy*; D011788:Quality of Life; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D051192:Receptors, Pattern Recognition
keywords: adverse remodeling; danger-associated molecular patterns; infarct size reduction; inflammation; myocardial infarction; pattern-recognition receptors