Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA.
Proc Am Thorac Soc. 2012 Jul;9(3):102-10. doi: 10.1513/pats.201201-005AW.
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.
异常的伤口愈合反应被认为对肺纤维化疾病（如特发性肺纤维化（IPF））有贡献。溶血磷脂酸（LPA）和鞘氨醇 1-磷酸（S1P）等溶血磷脂由于其介导许多基本细胞功能的能力，包括存活、增殖、迁移和收缩，可以影响伤口愈合所涉及的许多生物学过程。因此，最近的研究表明，LPA 和 S1P 可能在调节肺纤维化的发展中起关键作用。在这里，我们回顾了表明 LPA 和 S1P 调节肺纤维化的证据，以及这些溶血磷脂可能通过何种潜在机制影响肺损伤引起的纤维化。
