We explored the impact of 1,25-dihydroxyvitamin D3 (VD3) on heart health, particularly after an acute myocardial infarction (AMI). To investigate this, we used male C57/BL6J mice and conducted a series of experiments, comparing those treated with VD3 to control groups.
Our findings revealed that VD3 treated mice showed significant improvement in heart function following AMI. This treatment not only enhanced cardiac function parameters but also reduced inflammation and the extent of myocardial damage. There was a notable decline in inflammatory markers and a decrease in cell apoptosis, indicated by a rise in protective proteins and a fall in those that lead to cell death.
In our in vitro studies with cardiomyocytes, we observed that VD3 boosted autophagy markers, enhancing the body’s ability to manage damaged cells. It seemed to activate key pathways involved in cell survival and repair, specifically the PI3K/AKT/mTOR pathway. However, when we inhibited this pathway with 3-methyladenine, the benefits of VD3 were reversed, indicating a direct link between autophagy promotion and the protective effects of VD3.
In summary, our research indicates that VD3 can be a valuable ally in the fight against heart damage and inflammation after a heart attack, primarily by supporting cellular repair processes.