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Fig. 6

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ZDB-IMAGE-221214-327
Source
Figures for Chen et al., 2021
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Figure Caption

Fig. 6 Molecular mechanism of post-exercise regulation of cardiac hypertrophy in zebrafish. (1) Due to the requirement of a large amount of energy supply under training conditions, the mitochondria need to keep homeostasis between energy production and consumption. (2) Mitochondrial function enhancement: aerobic exercise also activated prkaa1-pargc1a signaling, which enhanced mitochondrial biogenesis, division, fusion, and autophagy processes, thus improving mitochondrial function. (3) Elevated cardiac energy metabolic function: a large amount of energy is consumed during aerobic exercise. acads, acsl1b, and acsl2 lipolytic metabolizing enzymes are also activated for expression; (4) improve antioxidant capacity: as exercise generates ROS, excessive ROS can cause damage to organelles and DNA. At the same time, antioxidant genes such as HO1-SOD and SESN1 are activated to scavenge ROS (Created with BioRender.com)

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