used dihydroartemisinin to intervene in a fibrotic cell model established using a human embryonic lung fibroblast cell line and found that dihydroartemisinin inhibited cell viability, decreased Fe 2+ levels, and inhibited the expression of ferritin heavy chain 1 (FTH1) and nuclear receptor coactivator 4 (NCOA4) genes and proteins
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Studies have indeed demonstrated that hyperhomocysteinemia compromises microvascular function in various organs, including the microvascular system within the kidneys [60]
