The Molecular Mechanisms Associated with Aerobic Exercise-Induced Cardiac Regeneration

Figures

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  Figure 1. Schematic of exercise-induced cardiac hypertrophy. Aerobic and anaerobic exercise elicits physiological cardiac remodeling. Hypertrophy activation is principally eccentric for aerobic but concentric for anaerobic exercise. LA, left atrium; LV, left ventricle; LVWT, left ventricular wall thickness; RA, right atrium; RV, right ventricle.

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  Figure 2. Schematic of major signaling pathways and other factors involved in aerobic exercise-induced cardiomyocyte regeneration. IGF-1 and neuregulin-1 activate PI3K and downstream Akt signaling pathways. Akt activates 4EBP1 and S6K1, downstream signaling molecules of mTOR, which act as crucial factors governing protein biosynthesis in the process of cardiac growth. C/EBPβ and downstream CITED4 are activated by Akt1 and are responsible for cardiomyocyte proliferation. Sirt1 and PGC-1α promote mitochondrial biogenesis. MiR-222 and miR-17-3p have also been shown to regulate the cell cycle and cardiomyocyte proliferation. Akt, RAC-α serine/threonine-protein kinase; C/EBPβ, CCAAT/enhancer-binding protein-β; CITED4, CBP/p300-interacting transactivator with ED-rich carboxy-terminal domain-4; eIF4E, translation initiation factor 4E; IGF-1, insulin growth factor-1; mTOR, mammalian target of rapamycin; PDK1, phosphoinositide-dependent protein kinase-1; PGC-1α, peroxisome proliferator-activated receptor-γ coactivator 1α; PI3K, phosphoinositide 3-kinase; Sirt1, NAD-dependent deacetylase sirtuin1; S6K1, ribosomal protein S6 kinase-β1; 4EBP1, eIF4E-binding protein 1.