

Industry-leading capabilities for heart failure research

Precisely recapitulates core pathogenic mechanisms of human Alport syndrome.
Homozygous knockout of Col4a3 disrupts the α3 chain of type IV collagen in the glomerular basement membrane, mirroring the genetic basis of hereditary Alport syndrome in patients.
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Spontaneous, Progressive Disease Course
Chemical induction is not required for model establishment. As animals age, they spontaneously develop persistent proteinuria, glomerulosclerosis, tubulointerstitial fibrosis, and progressive renal function decline—faithfully replicating the human disease trajectory from microalbuminuria to severe proteinuria and ultimately end-stage renal failure.
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Comprehensive heart failure models for preclinical research
Explore our validated heart failure studies demonstrating the efficacy of various therapeutic interventions.
Browse our comprehensive catalog of over 30,000 mouse models covering various gene families, signaling pathways, and disease models. Use advanced filters to find the perfect model for your research.
Discover related models and services to accelerate your cardiovascular research

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