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Whether homocysteine-lowering strategies (e.g., folate/B 12 or betaine therapy) could mitigate vascular risks in thalassemia warrants further investigation, drawing parallels from homocystinuria and cardiovascular prevention strategies.In conclusion, our study highlights homocysteine as a crucial biochemical factor in pediatric thalassemia, closely linked to nutritional deficiencies and oxidative stress

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However controversy exists as to whether TMAO influences the progression of CVD disease or acts as a bystander of dysbiosis and pro-inflammatory pathways when examining CVD and T2D patients ( Trimethylamine N-oxide has been shown to induce endoplasmic reticulum (ER) stress through the elevation of ER-HSP70 isoform ( Elevated levels of TMAO have also been observed to inhibit mitochondrial electron transport, thus leading to mitochondrial uncoupling and ROS formation in vascular endothelial cells (Zhu et al., 2016)