Cardiac Fibrosis Mice
Since 1998, ingenious targeting laboratory has supported cardiovascular research with mouse model generation for studying cardiac fibrosis, myocardial remodeling, and heart failure.
Our cardiac fibrosis models have contributed to research on extracellular matrix remodeling, fibroblast activation, and anti fibrotic therapeutics. Cardiac fibrosis mouse models provide essential platforms for investigating the molecular pathways underlying myocardial fibrosis, testing hypotheses about fibroblast biology, and developing therapies for heart failure and cardiac remodeling.
Frequently asked questions
Common cardiac Cre drivers include Myh6-Cre (cardiomyocytes), Tcf21-MerCreMer (cardiac fibroblasts, inducible), Postn-Cre (activated fibroblasts), and SM22-Cre (smooth muscle cells). Selection depends on whether you're studying cardiomyocyte responses, fibroblast activation, or myofibroblast function in fibrosis.
Cardiac fibrosis can be modeled through pressure overload (transverse aortic constriction), myocardial infarction (coronary ligation), or genetic modifications affecting fibroblast activation or extracellular matrix production. Conditional approaches enable tissue specific study of genes involved in fibrosis without systemic effects.
Yes. Tamoxifen-inducible Cre (CreER) enables temporal control of gene deletion in cardiac fibroblasts or cardiomyocytes, allowing study of adult-onset fibrosis mechanisms without developmental effects. This is particularly useful for genes with essential developmental functions.
