Table 2 Application of Cu chelators in cuproptosis-related CNS diseases.
From: Copper homeostasis and cuproptosis in central nervous system diseases
Cu chelator | Type of model/subject | Mechanism | Ref |
|---|---|---|---|
TTM | Aβ/PS1 transgenic mice | Promotion of non-amyloidogenic protein production of AβPP | [147] |
TTM | BV-2 microglia | Reducing Inflammation by Inhibiting the TRAF6/AKT/NF-κB signaling pathway | [148] |
TTM | Transgenic mice expressing human mutant SOD1 | Reduces copper ion levels and inhibits lipid peroxidation | [93] |
D-penicillamine | AD patients | Reduces oxidative stress damage | [149] |
D-penicillamine | AD model In vitro | Solubilization of Cu-Aβ with assistance of nanoparticles | [150] |
D-penicillamine | Stroke | Improving myocardial function and reducing ischemic events | [151] |
D-penicillamine | Glioblastoma multiforme | Inhibits tumor cell proliferation through the TGF-β/Smad signaling pathway | [152] |
TETA | Transgenic mouse model of AD | Reduces BACE1 activity and mitigates amyloidosis | [153] |
Clioquinol | U87 glioblastoma cells | Induction of apoptosis and autophagy in glioblastoma | [154] |
Clioquinol | transgenic Huntington’s mice (R6/2) | Inhibition of HTT aggregation and reduction of striatal atrophy | [115] |
Clioquinol | Twenty AD patients | Reduces levels of CSF-Tau protein | [155] |
8-hydroxyquinoline | Glioma | Activates transcription factors in glioma cells and inhibits cell proliferation | [156] |
8-hydroxyquinoline | AD | Inhibits cholinesterase and reduces Aβ levels | [152] |
