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10.1513/pats.201201-005AW

http://scihub22266oqcxt.onion/10.1513/pats.201201-005AW
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C5455616!5455616 !22802282
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suck abstract from ncbi

pmid22802282
      Proc+Am+Thorac+Soc 2012 ; 9 (3 ): 102-10
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  • Role of the lysophospholipid mediators lysophosphatidic acid and sphingosine 1-phosphate in lung fibrosis #MMPMID22802282
  • Shea BS ; Tager AM
  • Proc Am Thorac Soc 2012[Jul]; 9 (3 ): 102-10 PMID22802282 show ga
  • Aberrant wound healing responses to lung injury are believed to contribute to fibrotic lung diseases, such as idiopathic pulmonary fibrosis (IPF). The lysophospholipids lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P), by virtue of their ability to mediate many basic cellular functions, including survival, proliferation, migration, and contraction, can influence many of the biological processes involved in wound healing. Accordingly, recent investigations indicate that LPA and S1P may play critical roles in regulating the development of lung fibrosis. Here we review the evidence indicating that LPA and S1P regulate pulmonary fibrosis and the potential mechanisms through which these lysophospholipids may influence fibrogenesis induced by lung injury.
  • |Capillary Permeability [MESH]
  • |Cell Physiological Phenomena [MESH]
  • |Epithelial Cells/metabolism [MESH]
  • |Fibroblasts/metabolism [MESH]
  • |Humans [MESH]
  • |Lysophospholipids/*metabolism [MESH]
  • |Pulmonary Alveoli/cytology/metabolism [MESH]
  • |Pulmonary Fibrosis/*metabolism [MESH]
  • |Receptors, Lysophosphatidic Acid/metabolism [MESH]
  • |Receptors, Lysosphingolipid/metabolism [MESH]
  • |Signal Transduction [MESH]
  • |Sphingosine/*analogs & derivatives/metabolism [MESH]


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