Exercise training affects calcium ion transport by downregulating the CACNA2D1 protein to reduce hypertension-induced myocardial injury in mice

Hypertension is a risk factor for cardiovascular disease, and exercise has cardioprotective effects on the heart. However, the mechanism by which exercise affects hypertension-induced myocardial injury remains unclear. Exercise response model of hypertension-induced myocardial injury in mice was analyzed using multiomics data to identify potential factors. The study found that serum Ca2+ and brain natriuretic peptide concentrations were significantly higher in the HTN (hypertension) group than in the control, HTN+MICT (moderate intensity continuous exercise), and HTN+HIIT (high intensity intermittent exercise) groups. Cardiac tissue damage and fibrosis increased in the HTN group, but exercise training reduced pathological changes, with more improvement in the HTN+HIIT group. Transcriptomic and proteomic studies showed significant differences in CACNA2D1 expression between the different treatment groups. HIIT ameliorated HTN-induced myocardial injury in mice by decreasing Ca2+ concentration and diastolizing vascular smooth muscle by downregulating CACNA2D1 via exercise. [Display omitted] •Ca2+ concentration increase can induce LAMA2 aggregation•High concentration of Ca2+ can promote the activity of ITGA7•HIIT can treat HTN in mice compared to MICT by downregulating CACNA2D1•Downregulating CACNA2D1 reduces Ca2+ concentration, improving myocardial damage Cardiovascular medicine; Kinesiology; Proteomics