Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis

  • Kaori Suzuki
    Department of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan
  • Etsuo A. Susaki
    Department of Biochemistry and Systems Biomedicine, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan
  • Isao Nagaoka
    Department of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Bunkyo-ku 113-8421, Tokyo, Japan

書誌事項

公開日
2022-09-22
資源種別
journal article
権利情報
  • https://creativecommons.org/licenses/by/4.0/
DOI
  • 10.3390/ijms231911148
公開者
MDPI AG

説明

<jats:p>Atherosclerosis is a chronic inflammatory disease of the vascular walls related to aging. Thus far, the roles of cellular senescence and bacterial infection in the pathogenesis of atherosclerosis have been speculated to be independent of each other. Some types of macrophages, vascular endothelial cells, and vascular smooth muscle cells are in a senescent state at the sites of atherosclerotic lesions. Likewise, bacterial infections and accumulations of lipopolysaccharide (LPS), an outer-membrane component of Gram-negative bacteria, have also been observed in the atherosclerotic lesions of patients. This review introduces the integration of these two potential pathways in atherosclerosis. Previous studies have suggested that LPS directly induces cellular senescence in cultured monocytes/macrophages and vascular cells. In addition, LPS enhances the inflammatory properties (senescence-associated secretory phenotype [SASP]) of senescent endothelial cells. Thus, LPS derived from Gram-negative bacteria could exaggerate the pathogenesis of atherosclerosis by inducing and enhancing cellular senescence and the SASP-associated inflammatory properties of specific vascular cells in atherosclerotic lesions. This proposed mechanism can provide novel approaches to preventing and treating this common age-related disease.</jats:p>

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