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. 2024 Sep 18;13(19):e036555. doi: 10.1161/JAHA.124.036555

Figure 3. Exercise improves IHD by facilitating intercellular communication.

Figure 3

Following ischemia, cell apoptosis ensues, cardiac fibrosis develops, and the inflammatory response is exacerbated during reperfusion. Exercise training can reduce apoptosis, inflammation and myocardial fibrosis following IR and promote vascular regeneration by improving mitochondrial redox balance. During exercise, exerkines are transported via exosomes to specific sites where they exert antiapoptotic functions through the increased expression of mitochondrial antioxidant enzymes, such as glutathione reductase, catalase. After exercise, the increase of antioxidant enzymes and the decrease inflammatory factors can reduce inflammation. Remarkably, swimming training make an elevated expression of PINK/Parkin and LC3‐I, which can modulate mitophagy to exert a similar anti‐inflammatory effect. Endurance exercise also enhances the ADP/ATP ratio, thereby promoting mitochondrial OXPHOS and reducing mitochondrial oxidative stress. The release of exerkines such as musclin, FGF21, FSTL1, and myonectin promote mitochondrial dynamics, biogenesis, and autophagy, which collectively contribute to angiogenesis and inhibit myocardial fibrosis. In this figure, exerkine FGF21 is taken as an example to illustrate its antifibrotic effect. Notably, exerkines play a crucial role in augmenting intercellular communication and ameliorating cardiovascular diseases. CAT indicates catalase; ERK, extracellular signal‐regulated protein kinase; FGF21, fibroblast growth factor 21; FSTL1, follistatin like 1; GR, glutathione reductase; GSH‐Px, glutathione peroxidase; HSP70, heat shock protein 70; IHD, ischemic heart disease; IL‐6, interleukin‐6; IR, ischemia–reperfusion; LC3, light chain 3; MMP2/9, matrix metalloproteinase‐2/9; p38 MAPK, p38 mitogen‐activated protein kinase; OXPHOS, oxidative phosphorylation; P, phosphorylation; PINK, PTEN‐induced putative kinase; Smad2/3, phospho Thr8; SOD, superoxide dismutase; TGF‐β, transforming growth factor‐beta; TLR4, toll‐like receptor 4; and TNF‐α, tumor necrosis factor‐alpha.