title: Update on the role of angiotensin in the pathophysiology of coronary atherothrombosis.
abstract: BACKGROUND
  Coronary atherothrombosis due to atherosclerotic plaque rupture or erosion is frequently associated with acute coronary syndromes (ACS). Significant efforts have been made to elucidate the pathophysiological mechanisms underlying acute coronary events.
  
  
  METHODS
  This narrative review is based on the material searched for and obtained via PubMed up to August 2014. The search terms we used were as follows: 'angiotensin, acute coronary syndromes, acute myocardial infarction' in combination with 'atherosclerosis, vulnerability, clinical trial, ACE inhibitors, inflammation'.
  
  
  RESULTS
  Among several regulatory components, the renin-angiotensin system (RAS) was shown as a key pathway modulating coronary atherosclerotic plaque vulnerability. Indeed, these molecules are involved in all stages of atherogenesis. Classically, the RAS is composed by a series of enzymatic reactions leading to the angiotensin (Ang) II generation and activity. However, the knowledge of RAS has expanded and become more complex. The discovery of novel components and their functions has revealed additional pathways that contribute to or counterbalance the actions of Ang II. In this review, we discussed on recent findings concerning the role of different angiotensin peptides in the pathophysiology of ACS and coronary atherothrombosis, exploring the link between these molecules and atherosclerotic plaque vulnerability.
  
  
  CONCLUSIONS
  Treatments selectively targeting angiotensins (including Mas and AT2 agonists, ACE2 recombinant, or Ang-(1-7) and almandine in oral formulations) have been tested in animal studies or in small human subgroups, expanding the perspective in the ACS prevention. These novel strategies, especially in the counter-regulatory axis ACE2/Ang-(1-7)/Mas, might be promising to reduce plaque vulnerability and inflammation.
authors.affiliation: Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva, Geneva, Switzerland.
authors.forename: Analina R
authors.initials: AR
authors.lastname: da Silva
authors.forename: Rodrigo A
authors.initials: RA
authors.lastname: Fraga-Silva
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Stergiopulos
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Montecucco
authors.forename: François
authors.initials: F
authors.lastname: Mach
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000809:Angiotensins / Q000037:antagonists & inhibitors / Q000502:physiology*; D017209:Apoptosis / Q000502:physiology; D001167:Arteritis / Q000209:etiology; D015415:Biomarkers / Q000378:metabolism; D049109:Cell Proliferation / Q000502:physiology; D003324:Coronary Artery Disease / Q000209:etiology*; D003328:Coronary Thrombosis / Q000209:etiology*; D006801:Humans; D009389:Neovascularization, Pathologic / Q000209:etiology; D058226:Plaque, Atherosclerotic / Q000209:etiology; D011945:Receptors, Angiotensin / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012422:Rupture, Spontaneous / Q000209:etiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D015415:Biomarkers; D011945:Receptors, Angiotensin
keywords: Acute coronary syndromes; angiotensin; atherosclerosis