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The results showed that the signal of OH (1:2:2:1) was very weak without the addition of GSH, but its signal was significantly enhanced with the addition of GSH, which was mainly due to the degradation of DCCMH under the action of GSH to release a large amount of Cu +

Abnormal levels of mitochondrial proteins in plasma neuronal extracellular vesicles in major depressive disorder

The oxidative phosphorylation of fatty acids at the mitochondria is essential for memory T-cell formation

The first medical report concerning the usage of DMSO as a pharmacological agent was published in 1964 [4]

STAT3 inhibition protects against neuroinflammation and BACE1 upregulation induced by systemic inflammation

SCD1 inhibition blocks the AKT-NRF2-SLC7A11 pathway to induce lipid metabolism remodeling and ferroptosis priming in lung adenocarcinoma