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      PAI-1 is a Marker and a Mediator of Senescence

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          Abstract

          Plasminogen Activator Inhibitor-1 (PAI-1) is a member of the evolutionarily conserved serine protease inhibitor (SERPIN) family, and a potent and rapid-acting inhibitor of both of the mammalian plasminogen activators. Organismal homeostasis requires physiological levels of endogenous PAI-1 and increased PAI-1 production guides the onset and progression of numerous human diseases and contributes to the multimorbidity of aging. Both chronological and stress-induced accelerated aging are associated with cellular senescence and accompanied by marked increases in PAI-1 expression in tissues. Recent studies suggest that PAI-1 is not only a marker but also a key mediator of cellular senescence and organismal aging. Here, we review the significance of PAI-1 as a bonafide marker as well as a critical mediator of cellular senescence associated with aging and aging-related pathologies.

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          Author and article information

          Journal
          9505803
          8623
          Arterioscler Thromb Vasc Biol
          Arterioscler. Thromb. Vasc. Biol.
          Arteriosclerosis, thrombosis, and vascular biology
          1079-5642
          1524-4636
          26 May 2017
          01 June 2017
          August 2017
          01 August 2018
          : 37
          : 8
          : 1446-1452
          Affiliations
          Feinberg Cardiovascular Research Institute, Feinberg School of Medicine Northwestern University, Chicago, Illinois
          Author notes
          [¥ ] Address for Correspondence: Douglas E Vaughan, MD, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, d-vaughan@ 123456northwestern.edu
          Article
          PMC5846199 PMC5846199 5846199 nihpa878825
          10.1161/ATVBAHA.117.309451
          5846199
          28572158
          c18b599e-6b1c-41e7-89ec-33c33a22b14b
          History
          Categories
          Article

          PAI-1,Senescence,Thrombosis,Arteriosclerosis,Endothelial dysfunction,Aging

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