![]() ![]() ![]() The most frequent medical cause of death in athletes is sudden cardiac death (SCD), which usually occurs during intensive training ( Harmon et al., 2014). 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. 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. ![]() FOXO proteins may be the core mediator of the regulatory network needed to promote the pathological response. 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. 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. 2Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, ChinaĮxercise-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.1Guangdong Cardiovascular Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.Zuoqiong Zhou 1† Lan Zheng 2† Changfa Tang 2† Zhanglin Chen 2 Runkang Zhu 2 Xiyang Peng 2* Xiushan Wu 1* Ping Zhu 1* ![]()
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