Clinical variation in patient responses to myocardial infarction (MI) has been difficult to model in laboratory animals. To assess the genetic basis of variation in outcomes after heart attack, we characterized responses to acute MI in the Collaborative Cross (CC), a multi-parental panel of genetically diverse mouse strains. Striking differences in post-MI functional, morphological, and myocardial scar features were detected across 32 CC founder and recombinant inbred strains. Transcriptomic analyses revealed a plausible link between increased intrinsic cardiac oxidative phosphorylation levels and MI-induced heart failure. The emergence of significant quantitative trait loci for several post-MI traits indicates that utilizing CC strains is a valid approach for gene network discovery in cardiovascular disease, enabling more accurate clinical risk assessment and prediction.

在实验室动物中很难模拟患者对心肌梗塞（MI）反应的临床差异。为了评估心脏病发作后结果变化的遗传基础，我们在协作性交叉（CC）（一种遗传多样性小鼠品系的多亲小组）中表征了对急性心肌梗死的反应。在32个CC创始者和重组自交系中检测到MI后功能，形态和心肌疤痕特征的显着差异。转录组学分析显示，内在的心脏氧化磷酸化水平升高与MI诱发的心力衰竭之间存在合理的联系。针对多种MI后性状的重要定量性状基因座的出现表明，利用CC菌株是在心血管疾病中发现基因网络的有效方法，