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's study separated rats into five groups, and the immunohistochemistry results indicate that DSS (0.5, 1.0, and 2.0 mg/kg) significantly increased Bcl-2 expression in the cerebral area, while simultaneously inhibiting the expression of Bax and caspase-3

However, more studies are still warranted for further exploration of other mechanistic molecular targets that may play role in the pathophysiology of cyclophosphamide-induced neurotoxicity such as involvement of protein oxidation and mitochondrial DNA damage in mediating this adverse effect

This explains why cancer cells have been shown to increase expression of amino acid transporters to take up large amounts of amino acids

Identification of a small molecule that enhances ferroptosis via inhibition of ferroptosis suppressor protein 1 (FSP1)

Epigenetic reprogramming of cancer-Associated fibroblasts deregulates glucose metabolism and facilitates progression of breast cancer