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In particular, damaged tubular cells are an important source of M2 macrophage polarization factors, such as macrophage colony-stimulating factor, granulocyte-macrophage colony stimulating factor, and Nectrin 1 (89)

Though epidemiological studies [12] and randomized trials [9] have suggested a possible reduction of cardiovascular risk factors following treatment, other animal and human studies have shown that L-C may increase pro-atherogenic metabolites such as trimethylamine oxide (TMAO) [13,14,15]

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What counts is both ineffective erythropoiesis and ferroptosis in -thalassemia are intricately linked to the iron metabolism and Reactive oxygen species homeostasis