Key result
Mouse gene profiling identifies DPPI and TIMP-3 as key drivers of early lung fibrosis inflammation.
Population
C57BL/6 (sensitive) and BALB/c (resistant) mice
Comparison
Intratracheal bleomycin instillation; genetic… vs Mice without bleomycin administration; wild-type…
Design
Preclinical
Authors
Loading...
Should not change clinical practice in pulmonary fibrosis; leaves open validation of DPPI and TIMP-3 as therapeutic targets in humans.
The study identifies DPPI and tissue inhibitor of matrix metalloproteinase-3 as key genes in the early inflammatory response to bleomycin, though DPPI deletion alone does not prevent fibrosis in sensitive mice.
Pottier et al. (2007) studied Bleomycin-induced lung fibrosis. Bleomycin instillation vs. BALB/c mice (resistant strain) was evaluated on Gene expression profiles and lung fibrosis development. Expression of 25 genes differed between sensitive and resistant mice, identifying DPPI and tissue inhibitor of matrix metalloproteinase-3 as key factors in early inflammatory events of lung fibrosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: