We explored the relationship between vitamin D deficiency and heart disease, particularly how it interacts with a condition called hyperhomocysteinemia, which is known to promote heart issues. In our study, we examined both animal models (rats fed a diet to induce hyperhomocysteinemia) and heart cells under lab conditions to understand this interaction better.
Our findings revealed that hyperhomocysteinemia significantly lowered levels of vitamin D, specifically 1,25(OH)D, in the blood and heart tissues. We also noted an increase in the expression of an enzyme (CYP24A1) that breaks down vitamin D, indicating a disruption in its availability. Moreover, the presence of elevated homocysteine was linked to a decrease in vitamin D receptor (VDR) expression in heart tissues, complicating the heart's ability to respond to vitamin D’s effects.
By manipulating levels of VDR, we demonstrated that reducing VDR led to more heart cell growth, which is a sign of heart hypertrophy. Conversely, when VDR was overexpressed, we observed a decrease in hypertrophy, showing that vitamin D plays a protective role against heart enlargement during hyperhomocysteinemia. Additionally, a specific microRNA (miR-125b-5p) was found to repress VDR and contribute to heart cell growth, highlighting the complex regulatory network involved.
Our study concluded that vitamin D deficiency and reduced VDR contribute to heart issues associated with high levels of homocysteine by activating harmful cellular pathways. This underscores the potential significance of monitoring and supporting vitamin D levels, especially in individuals suffering from hyperhomocysteinemia.