Duchenne muscular dystrophy (DMD) is a common fatal heritable myopathy, with cardiorespiratory failure occurring by the third decade of life. There is no specific treatment for DMD cardiomyopathy, in large part due to a lack of understanding of the mechanisms underlying the cardiac failure. Mdx mice, which have the same dystrophin mutation as human patients, are of limited use, as they do not develop early dilated cardiomyopathy as seen in patients. Here we summarize the usefulness of the various commonly used DMD mouse models, highlight a model with shortened telomeres like humans, and identify directions that warrant further investigation.

杜兴氏肌营养不良症（DMD）是一种常见的致命遗传性肌病，在生命的第三个十年出现心肺衰竭。没有针对DMD心肌病的特定治疗方法，这在很大程度上是由于对心力衰竭的潜在机制缺乏了解。具有与人类患者相同的肌营养不良蛋白突变的Mdx小鼠用途有限，因为它们不像患者那样发展为早期扩张型心肌病。在这里，我们总结了各种常用DMD鼠标模型的有用性，突出显示了具有像人类一样的端粒缩短的模型，并确定了值得进一步研究的方向。