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      Inflammasome activation by mitochondrial oxidative stress in macrophages leads to the development of angiotensin II-induced aortic aneurysm.

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          Abstract

          Abdominal aortic aneurysm (AAA) is considered a chronic inflammatory disease; however, the molecular basis underlying the sterile inflammatory response involved in the process of AAA remains unclear. We previously showed that the inflammasome, which regulates the caspase-1-dependent interleukin-1β production, mediates the sterile cardiovascular inflammatory responses. Therefore, we hypothesized that the inflammasome is a key mediator of initial inflammation in AAA formation.

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          Author and article information

          Journal
          Arterioscler. Thromb. Vasc. Biol.
          Arteriosclerosis, thrombosis, and vascular biology
          1524-4636
          1079-5642
          Jan 2015
          : 35
          : 1
          Affiliations
          [1 ] From the Division of Inflammation Resesarch, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan (F.U., K.S., H.K., K.T., A.K., T.K., M.T.); Department of Molecular Oncology, Shinshu University Graduate School of Medicine, Matsumoto, Japan (J.S., S.T.); Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan (K.Y.); Cardiovascular Research Institute, Kurume University, Kurume, Japan (H.A.); Department of Microbiology, Hyogo College of Medicine, Nishinomiya, Japan (H.T.); and Department of Cell Biology, Japanese Foundation for Cancer Research, Cancer Institute, Tokyo, Japan (T.N.).
          [2 ] From the Division of Inflammation Resesarch, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan (F.U., K.S., H.K., K.T., A.K., T.K., M.T.); Department of Molecular Oncology, Shinshu University Graduate School of Medicine, Matsumoto, Japan (J.S., S.T.); Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan (K.Y.); Cardiovascular Research Institute, Kurume University, Kurume, Japan (H.A.); Department of Microbiology, Hyogo College of Medicine, Nishinomiya, Japan (H.T.); and Department of Cell Biology, Japanese Foundation for Cancer Research, Cancer Institute, Tokyo, Japan (T.N.). masafumi2@jichi.ac.jp.
          Article
          ATVBAHA.114.303763
          10.1161/ATVBAHA.114.303763
          25378412
          ae6cfd40-8fcd-4ca6-91f2-14578e583e58
          © 2014 American Heart Association, Inc.
          History

          cytokines,inflammation,macrophages,oxidative stress
          cytokines, inflammation, macrophages, oxidative stress

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