Key result
Excessive exercise drives pathological cardiac hypertrophy in zebrafish, altering ~3,082 mRNAs linked to autophagy.
Why the study?
Exercise-induced cardiac remodeling is a concern due to sudden cardiac death in athletes, but little is known about the underlying mechanism of exercise-induced cardiac injury.
p-value: p=<0.05
This preclinical study identifies key genes and pathways, including FOXO signaling, involved in excessive exercise-induced pathological cardiac hypertrophy in a zebrafish model.
Highlights autophagy/FoxO pathways in over-exercise hypertrophy; leaves open translation to human athletes.
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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Zhou et al. (2020) studied Excessive exercise-induced pathological cardiac hypertrophy (n=60). Excessive exercise (swimming training) vs. Static control (remained in housing tanks) was evaluated on Differentially expressed mRNAs (p=<0.05). Excessive exercise induced pathological cardiac hypertrophy in zebrafish and resulted in 3,082 differentially expressed mRNAs primarily involved in autophagy, protein homeostasis, and FoxO signaling.
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