Animal models of cardiac fibrosis.

A collagen network, composed largely of type I and III fibrillar collagens, is found in the heart's interstitial space. This network has multiple functions, including the preservation of tissue architecture and chamber geometry. Given its tensile strength, type I collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, expressed in morphological terms as tissue fibrosis, increases myocardial passive and active stiffness and contributes to ventricular diastolic and systolic dysfunction. Various animal models of cardiac fibrosis have been used to study its functional consequences and to elucidate factors regulating the cellular and molecular biology of fibrogenesis. Herein, we present our experience and findings with several models of cardiac fibrosis.