HYDERABAD: Vitamin D deficiency may trigger cellular stress responses in the heart that can lead to cardiac cell damage and death, a study by researchers at the ICMR-National Institute of Nutrition (ICMR-NIN), Hyderabad, has found.
Published in Steroids, the study examined vitamin D deficiency and insufficiency in male rats and the H9C2 rat cardiomyoblast cell line, focusing on oxidative and nitrosative stress, antioxidant defences, Nrf2 signalling, endoplasmic reticulum (ER) stress, autophagy and apoptosis.
Rats fed vitamin D-deficient diets showed increased oxidative damage, including lipid peroxidation and DNA damage, along with reduced levels of reduced glutathione and key antioxidant enzymes. Researchers also observed increased Nox2 expression, indicating a more pro-oxidant environment.
Vitamin D deficiency impaired the Nrf2 antioxidant pathway and increased markers of ER stress. Higher levels of pro-apoptotic proteins BAX and BIM, along with reduced BCL2, indicated increased apoptotic signalling. “We further observed increased markers of endoplasmic reticulum (ER) stress, autophagy and apoptosis in vitamin D-deficient hearts. These findings suggest that prolonged oxidative stress associated with inadequate vitamin D may trigger a cascade of cellular responses that can contribute to cardiac cell injury,” said Dr Ayesha Ismail, Scientist F, who led the research group.
Experiments on H9C2 cells showed that oxidative stress reduced cell viability and increased markers of oxidative damage, ER stress, autophagy and apoptosis. Pretreatment with the active form of vitamin D improved cell viability and antioxidant responses while reducing these markers.
The researchers proposed that vitamin D deficiency may disrupt redox balance, triggering ER stress, altered autophagy and programmed cardiac cell death. However, the study was limited to male rats and cell models, and further research is needed to determine whether the findings apply directly to humans.
