Key result
Mice lacking JNK1 accumulated less subepithelial collagen deposition and were protected against TGF-beta1 and bleomycin-induced pulmonary fibrosis compared with wild-type mice.
Why the study?
Does JNK1 deficiency prevent collagen deposition and pulmonary fibrosis in mouse models?
Population
Mice subjected to models of allergic airways disease and interstitial pulmonary fibrosis
Comparison
JNK1 genetic deletion (JNK1-/- mice) vs Wild-type (WT) mice
Design
Preclinical
Authors
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JNK1 merits exploration as an antifibrotic target; leaves open translation from murine models to human pulmonary fibrosis.
Does JNK1 deficiency prevent collagen deposition and pulmonary fibrosis in mouse models?
JNK1 is required for promoting collagen deposition and pulmonary fibrosis in multiple mouse models, suggesting it as a potential therapeutic target.
Alcorn et al. (2008) studied Pulmonary fibrosis and allergic airways disease. JNK1 deficiency (JNK1-/-) vs. Wild-type (WT) mice was evaluated on Subepithelial collagen deposition and pro-fibrotic gene expression. Mice lacking JNK1 accumulated less subepithelial collagen deposition and were protected against TGF-beta1 and bleomycin-induced pulmonary fibrosis compared with wild-type mice.
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