Cardiomyopathic BIO hamsters are excellent animal models for heart failure and for gene therapy in myopathies

Abstract

A spontaneous mutation affecting the striatal muscle in a Syrian hamster strain was discovered in 1959 (Homburger et al, New hereditary disease of Syrian hamsters. Primary, generalized polymyopathy and cardiac necrosis, Arch Intern Med. 1962;110:–2). Subsequent research over the past many years has revealed that this mutation in BIO hamsters is confined to a single autosomal-recessive gene that affects all muscle systems (striated, smooth and cardiac muscles). Currently, there are two distinctly different yet related myopathic BIO hamster strains (BIO 14.6 & BIO TO-2) and these are widely being used as animal models for autosomal recessive cardiomyopathy. One important feature of these hamsters is premature death due to progressive myocardial necrosis and eventual heart failure. At the molecular level, the defective gene has been identified as being related to the delta-sarcoglycan gene and this finding has stimulated a great deal of interest in gene therapy in diseases involving the three muscle groups (striated, smooth and cardiac). While there is an extensive literature on these BIO hamster models for various applications, there is a need to provide updated information on their characteristics as compared with control BIO hamsters. These include physical measurements such as body weight changes throughout their life span, survival curves, blood chemistries including lipid profiles, and hemodyamics. Additional applications for these BIO hamster models are also being recognized.