Cardiac Fibrosis Mice

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.