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The metabolic adaptive mechanism has introduced new challenges to treatment, and there is an urgent need to develop a joint treatment strategy that targets multiple key metabolic nodes simultaneously

There was no basal level difference in MDA levels in IB3-1 and C38 (Fig

Thus, while both toxin models capture essential elements of demyelination-associated activation, neither fully recapitulates the spectrum of microglial heterogeneity present in human disease

Moreover, by targeting ferroportin, miR-302a-3p can induce lipid peroxidation and iron overload, inhibit the growth and colony formation of lung cancer cells, and increase their sensitivity to CDDP and paclitaxel chemotherapy [153]