Construction of a Zebrafish Model of Cardiac Hypertrophy Caused by ATIC Gene Deletion and Preliminary Exploration of Aerobic Exercise Improvement

构建ATIC基因缺失引起的斑马鱼心脏肥大模型及有氧运动改善作用的初步探索

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Abstract

Hypertrophic cardiomyopathy (HCM) is a relatively common global cardiac disease, usually inherited, with complex phenotypes, genetic features, and a natural history. In this study, we constructed atic(-/-) zebrafish using the CRISPR/Cas9 gene-editing system and found that atic(-/-) zebrafish hearts exhibited HCM symptoms, and atic(-/-) zebrafish hearts showed progressive enlargement, eccentric hypertrophy, cardiomyocyte enlargement, and collagen fiber deposition. Echocardiography results also showed that compared with atic(-/-) zebrafish hearts, in wild-type zebrafish hearts, the ejection fraction was significantly reduced, shortening fraction was reduced, and ventricular wall thickness was significantly increased. Meanwhile, aerobic exercise intervention in atic(-/-) zebrafish showed that aerobic exercise effectively improved the symptoms of HCM and improved cardiac function in atic(-/-) zebrafish hearts. Transcriptome sequencing results showed that aerobic exercise improved the symptoms of HCM in atic(-/-) zebrafish hearts involving the calcium signaling pathway, Apelin signaling pathway and ECM-receptor interaction. The q-PCR results of key differential genes involved in these pathways further confirmed that aerobic exercise could bring beneficial effects to atic(-/-) zebrafish. In conclusion, this study found that the loss of ATIC can lead to hypertrophic cardiomyopathy in zebrafish, and aerobic exercise intervention can effectively improve the hypertrophic pathological characteristics of atic(-/-) zebrafish hearts, providing new intervention targets and effective lifestyle interventions for HCM.

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