期刊
FRONTIERS IN PHYSIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2020.565307
关键词
pathological cardiac hypertrophy; RNA-seq; autophagy; FoxO signaling pathway; excessive exercise
类别
资金
- National Key Research and Development Program of China [2018YFA0108700, 2017YFA0105602]
- NSFC Projects of International Cooperation and Exchanges [81720108004]
- National Natural Science Foundation of China [32071175, 81801392, 81570279, 81974019, 81670290]
- Research Team Project of Natural Science Foundation of Guangdong Province of China [2017A030312007]
- Key Program of the Guangzhou Science Research Plan [201904020047]
- Special Project of the Dengfeng Program of Guangdong Provincial PeopleSs Hospital [DFJH201812, KJ012019119, KJ012019423]
- Hunan Provincial Natural Science Foundation of China [2020JJ5354]
- Postgraduate Scientific Research Innovation Project of Hunan Province [CX20200532]
Exercise-induced cardiac remodeling has aroused public concern for some time, as sudden cardiac death is known to occur in athletes; however, little is known about the underlying mechanism of exercise-induced cardiac injury. In the present study, we established an excessive exercise-induced pathologic cardiac hypertrophy model in zebrafish with increased myocardial fibrosis, myofibril disassembly, mitochondrial degradation, upregulated expression of the pathological hypertrophy marker genes in the heart, contractile impairment, and cardiopulmonary function impairment. High-throughput RNA-seq analysis revealed that the differentially expressed genes were enriched in the regulation of autophagy, protein folding, and degradation, myofibril development, angiogenesis, metabolic reprogramming, and insulin and FoxO signaling pathways. FOXO proteins may be the core mediator of the regulatory network needed to promote the pathological response. Further, PPI network analysis showed that pik3c3, gapdh, fbox32, fzr1, ubox5, lmo7a, kctd7, fbxo9, lonrf1l, fbxl4, nhpb2l1b, nhp2, fbl, hsp90aa1.1, snrpd3l, dhx15, mrto4, ruvbl1, hspa8b, and faub are the hub genes that correlate with the pathogenesis of pathological cardiac hypertrophy. The underlying regulatory pathways and cardiac pressure-responsive molecules identified in the present study will provide valuable insights for the supervision and clinical treatment of pathological cardiac hypertrophy induced by excessive exercise.
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