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Allograft inflammatory factor-1, a multi-target regulator of atherosclerosis

  • Yujiao Zhang
    Affiliations
    Université de Paris, INSERM UMR-S 970, Paris Cardiovascular Research Center, PARCC, Paris, France
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  • Alain Tedgui
    Affiliations
    Université de Paris, INSERM UMR-S 970, Paris Cardiovascular Research Center, PARCC, Paris, France
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  • Hafid Ait-Oufella
    Correspondence
    Corresponding author. UMR-S 970 Paris Cardiovascular Research Center, PARCC, 56 Rue Leblanc, 75015, Paris, France.
    Affiliations
    Université de Paris, INSERM UMR-S 970, Paris Cardiovascular Research Center, PARCC, Paris, France
    Service de Médecine Intensive-réanimation, Hôpital Saint-Antoine, Assistance Publique-Hôpitaux de Paris, Sorbonne-Université, Paris, France
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      Atherosclerosis is a chronic inflammatory disease of the arterial wall responsible for ischemic heart disease and stroke, the most frequent causes of death worldwide. Cardiovascular diseases are expected to remain the main cause of death globally within the next 15 years, owing to a rapidly increasing prevalence, mainly due to the rising incidence of obesity and diabetes on a global scale in both developed and developing economies. This forces us to consider new strategies for prediction, prevention, and treatment of cardiovascular disease [
      • Libby P.
      • Hansson G.K.
      Taming immune and inflammatory responses to treat atherosclerosis.
      ]. There is a large body of human and experimental evidence showing that the innate immune response, mainly through monocytes/macrophages, is involved in the initiation and progression of atherosclerosis, as well as in its complications such as plaque rupture and resulting acute myocardial infarction. Infiltrating monocytes/macrophages act like Dr. Jekyll/Mr. Hyde playing a dual role depending on the stage of atherosclerosis. Monocytes/macrophages are known to accelerate atherosclerosis plaque growth through the release of chemokines, cytokines, cell death and defective efferocytosis [
      • Van Vre E.A.
      • Ait-Oufella H.
      • Tedgui A.
      • Mallat Z.
      Apoptotic cell death and efferocytosis in atherosclerosis.
      ]. However, they also exhibit atheroprotective functions through lipid uptake and cell debris scavenging. In this issue of Atherosclerosis, Egana-Gorrono et al. report that Allograft Inflammatory Factor-1 (Aif-1) deficiency had no impact on the size of advanced atherosclerotic plaques, but the lipid-rich necrotic core, a marker of plaque vulnerability, was larger [
      • Egana-Gorrono L.
      • Chinnasamy P.
      • Casimoro I.
      • Almonte V.M.
      • Parikh D.
      • Oliveira-Paula G.H.
      • Jayakumar S.
      • Law C.
      • Riascos-Bernal D.F.
      • Sibinga N.E.S.
      Allograft inflammatory factor-1 supports macrophage survival and efferocytosis and limits necrosis in atherosclerotic plaques.
      ].
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