Open AccessTSP‐1 in lung fibrosis
Author(s) -
Di Guglielmo Gianni M.
Publication year - 2010
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-010-0097-8
Subject(s) - bleomycin , lung , pulmonary fibrosis , fibrosis , thrombospondin 1 , medicine , cytokine , lung fibrosis , transforming growth factor , immunology , transforming growth factor beta , tgf beta signaling pathway , cancer research , pathology , chemotherapy , angiogenesis
Lung fibrosis is often treated with corticosteroids to reduce the inflammatory response, however, no effective treatment options exist for the underlying disease. An important player in the fibrotic cascade is the cytokine, transforming growth factor beta (TGFβ). TGFβ is converted from an inactive procytokine complex to active TGFβ by enzymes such as thrombospondin‐1 (TSP‐1). It is therefore presumed that TSP‐1 deficient mice would fare better to bleomycin‐induced pulmonary fibrosis because TGFβ would not be efficiently converted to the active form. Interestingly, a recent article by Ezzie and colleagues shows that TSP‐1 deficiency does not protect mice from systemic bleomycin challenge. Indeed, they find the opposite, as TSP‐1‐null mice appear to exhibit greater lung fibrosis than wild type mice, although similar TGFβ signaling was observed in the lungs of both mouse strains.