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Adverse effects on these organelles are the prime culprits of following apoptosis in endothelial cells. Fortunately, additional antioxidants and calcium inhibitors could mitigate cellular lesion through improvement of subcellular function. Intriguingly, antioxidants relieve cell stress via both mitochondrial and ER stress-mediated pathways, whereas the role of calcium modulators in cell apoptosis is independent of the mitochondrial pathway but could be explained by amelioration of ER stress. In conclusion, our data bas

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