This study investigates the role of IGFBP2 in alveolar epithelial type 2 (AEC2) cell senescence and lung fibrosis. Loss of IGFBP2 leads to increased cellular senescence and fibrotic markers. Conversely, overexpression of human IGFBP2 in AEC2 cells reduces fibrosis in a bleomycin-induced lung injury model.
IGFBP2 deficiency enhances AEC2 senescence and SASP production, exacerbating lung fibrosis. AEC2-specific restoration of IGFBP2 reduces fibrosis and inflammation, supporting its therapeutic relevance in pulmonary fibrosis.
Conditional Knockin mouse model developed by genOway, with human IGFBP2 cDNA inserted into the Rosa26 locus. Expression is driven by Sftpc-CreERT2 for AEC2-specific and tamoxifen-inducible activation.
Pulmonary fibrosis, Alveolar epithelial cells, Senescence, IPF, AEC2-targeted therapy
Conditional Knockin model, Rosa26 locus targeting, Sftpc-CreERT2 driver, Tamoxifen induction, Human IGFBP2 expression
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
