We demonstrated that modifications in the abundance of the signaling sphingolipid ceramide trigger a cascade of events that culminates in emphysema-like disease in animals. To rebalance the sphingolipid homeostasis, we recently demonstrated that augmentation of endothelial pro-survival signaling with sphingosine-1 phosphate agonists is effective in preventing lung structural cell apoptosis and airspace enlargement.

Selected related publications

  • Justice, M. J. et al. Effects of lipid interactions on model vesicle engulfment by alveolar macrophages. Biophysical journal 106, 598-609, doi:10.1016/j.bpj.2013.12.036 (2014).
  • Petrache, I. et al. Ceramide synthases expression and role of ceramide synthase-2 in the lung: insight from human lung cells and mouse models. PloS one 8, e62968, doi:10.1371/journal.pone.0062968 (2013).
  • Kamocki, K. et al. RTP801 is required for ceramide-induced cell-specific death in the murine lung. American journal of respiratory cell and molecular biology 48, 87-93, doi:10.1165/rcmb.2012-0254OC (2013).
  • Petrache, I. et al. Ceramide causes pulmonary cell apoptosis and emphysema: a role for sphingolipid homeostasis in the maintenance of alveolar cells. Proceedings of the American Thoracic Society 3, 510, doi:10.1513/pats.200603-071MS (2006).
  • Petrache, I. et al. Ceramide upregulation causes pulmonary cell apoptosis and emphysema-like disease in mice. Nature medicine 11, 491-498, doi:10.1038/nm1238 (2005).
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