At birth, mice homozygous for both targeted alleles are viable, normal in size and do not display any gross physical or behavioral abnormalities. All double mutants die between 5 to 8 weeks following birth, exhibiting hypercholesterolemia and significantly lower body weights compared to control mice. Mice display an altered appearance several days before death, displaying ruffled fur, an abnormal gate and sometimes labored breathing. Hearts from double mutants are enlarged, exhibit evidence of myocardial infarction and are functionally impaired. Histological examination reveals extensive coronary artery disease characterized by atherosclerotic plaques with evidence of cholesterol clefts and fibrin deposition. As with other <em>Scarb1</em> homozygous null mutants, females are infertile while the fertility of homozygous males remains intact. This double mutant mouse strain offers a model that may be a useful tool in studies related to coronary heart disease. 

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These SR-BI/apoE double knock-out mice exhibit hypercholesterolemia, low body weights, and early mortality.

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