Selected article for: "acute lung injury and lung injury acute"
Author: Jorge Blazquez-Prieto; Covadonga Huidobro; Ines Lopez-Alonso; Laura Amado-Rodriguez; Paula Martin-Vicente; Cecilia Lopez-Martinez; Irene Crespo; Cristina Pantoja; Pablo J Fernandez-Marcos; Manuel Serrano; Jacob I Sznajder; Guillermo M Albaiceta
Title: Cellular senescence limits acute lung injury induced by mechanical ventilation
  • Document date: 2020_3_25
    • ID: ebwxryai_63
    Snippet: Activation of a senescence cell program has been shown in several models of lung diseases. Lipopolysaccharide or bleomycin-induced lung injury increases the number of SA-b-galactosidase-positive cells and leads to cell cycle arrest (24) . It has been shown that this activation has no detrimental effects in acute inflammation. The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.24.005983 do.....
    Document: Activation of a senescence cell program has been shown in several models of lung diseases. Lipopolysaccharide or bleomycin-induced lung injury increases the number of SA-b-galactosidase-positive cells and leads to cell cycle arrest (24) . It has been shown that this activation has no detrimental effects in acute inflammation. The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.24.005983 doi: bioRxiv preprint However, blockade of the cell cycle has been associated with increased collagen deposition (25) and SASP may perpetuate lung inflammation (26) . Therefore, main features of abnormal lung repair after acute injury (limited cell proliferation, chronic inflammation and fibrosis) could be explained by a persistent senescent response. Inhibition of this response by selective deletion of Tp53 in Club cells ameliorated lung damage related to chronic inflammation (24) , suggesting a novel mechanism amenable to treatment of lung diseases.

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