Aerobic Exercise-Assisted Cardiac Regeneration by Inhibiting Tryptase Release in Mast Cells after Myocardial Infarction

Abstract

Background. Cardiovascular disease (CVD) contributes critically to the mortality, morbidity, and economic problem of illness globally. Exercise is a share of everyone’s life. Some evidence-based studies have frequently shown a progressive correlation between physical activity and good health. Objective. The effects of daily exercise on cardiomyocyte size, collagen content (fibrosis), and releasing mast cells (MCsʼ) tryptase of the model of myocardial infarction (MI) were assessed. Methods. 40 rats were coincidentally spread into sham+inertia (control), sham+exercise, infarction+inertia, and infarction+exercise groups. An experimental model of acute MI was induced in infarction groups. One week after surgery, exercising groups were allowed to an aerobic exercise program for six weeks. At the endpoint of the study, all examinations were performed. Results. We found lesser fibrosis in sham+exercise and infarction+exercise groups compared to sham+inertia and infarction+inertia groups, respectively ( p = 0.023 , p = 0.001 ). Also, infarction groups were significantly lower than sham groups ( p < 0.05 ) and the infarction+exercise group was significantly lower than the infarction+inertia group ( p < 0.05 ). The effect of exercise on MCs while increased MC density and degranulation occur at the site of fibrosis, we demonstrated that exercise decreases both total MC density and degranulation in both sham and infarction groups ( p < 0.05 ). Immunohistochemistry examinations were significantly higher expression of MCsʼ tryptase in infarction groups than sham groups ( p < 0.05 , p < 0.0001 ). Conclusion. Exercise improves fibrosis and cardiac function in both healthy and MI rats by inhibiting released MCsʼ tryptase.

Comprehensive bioinformatics analysis reveals the role of cuproptosis-related gene Ube2d3 in myocardial infarction

“…Additionally, atorvastatin has been shown to inhibit TLR-4/NF-κB activation after MI by inducing tolerogenic dendritic cells to improve myocardial remodeling ( 30 ). Furthermore, exercise has been found to enhance fibrosis and cardiac function in MI rats by inhibiting mast cell-released trypsin ( 31 ). The relationship between Ube2d3 and immune cells is relatively understudied, but existing knowledge indicates that Ube2d3 activates the NF-κB pathway to promote chemokine production and myeloid cell invasion in tumors ( 32 ).…”

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

“…Moreover, exercise training increases FGF 21 and regulates the TGF-β1-smad2/3-MMP2/9 axis ( Ma et al, 2021 ) and expression of lncRNAs H19, GAS5, and MIAT to decrease fibrosis in MI mice ( Farsangi et al, 2021 ). Additionally, exercise inhibits tryptase release by mast cells and cardiac fibrosis ( Bayat et al, 2021 ). The preconditioning with high-intensity interval training decreases heart injuries by increasing G-CSF and G-CSFR in the MI mouse model ( Ghanimati et al, 2020 ).…”