2022
DOI: 10.1016/j.ejphar.2022.175133
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Therapeutic Insights on Ferroptosis in Parkinson's disease

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Cited by 36 publications
(19 citation statements)
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“…NRF2 also regulates mitochondrial function and the expression of a variety of antioxidant genes. 46 After entering the nucleus, NRF2 binds to the antioxidant reaction element 11 (ARE11), which induces the expression of downstream antioxidant enzymes, such as GPX4 and superoxide dismutase (SOD) (Figure 3A). [47][48][49] Although the system xc − antiporter is the primary mechanism by which cells obtain cysteine, the transsulfuration pathway, which is dictated by the presence or absence of functional DJ-1, is a secondary mechanism.…”
Section: F I G U R Ementioning
confidence: 99%
See 1 more Smart Citation
“…NRF2 also regulates mitochondrial function and the expression of a variety of antioxidant genes. 46 After entering the nucleus, NRF2 binds to the antioxidant reaction element 11 (ARE11), which induces the expression of downstream antioxidant enzymes, such as GPX4 and superoxide dismutase (SOD) (Figure 3A). [47][48][49] Although the system xc − antiporter is the primary mechanism by which cells obtain cysteine, the transsulfuration pathway, which is dictated by the presence or absence of functional DJ-1, is a secondary mechanism.…”
Section: F I G U R Ementioning
confidence: 99%
“…Separately, in two randomized, double‐blind, placebo‐controlled phase II clinical trials, DFP reduced iron deposition in SN and progression of dyskinesia in early‐onset PD patients ( n = 19, NCT00943748; n = 22, NCT01539837) 91,92 . It should be noted that, low doses of DFP (15–30 mg/kg) were used in these clinical trials to prevent excess systemic iron chelation and associated adverse effects 46 . Moreover, DFP was the subject of two additional parallel‐group, placebo‐controlled, randomized phase II clinical trials focused on PD, the results of which are still pending ( n = 140, NCT02728843; n = 372, NCT02655315) 93,94 .…”
Section: Ferroptosis‐related Therapeutic Targets For Pdmentioning
confidence: 99%
“…Alterations in iron homeostasis promote the pathophysiological effects observed in several neurodegenerative diseases [ 106 , 107 , 108 ]. Furthermore, the occurrence of ferroptosis as a type of recent cell death has been receiving increased attention given its apparent occurrence in neurodegenerative diseases and the positive effect of inhibitors of this process in the disease progression [ 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 ]. Targeting ferroptosis can thus be proposed as a potential new therapeutic target to stop/delay neurodegenerative disease progression.…”
Section: Neurodegenerative Diseasesmentioning
confidence: 99%
“…Recent approaches using intranasal DFO treatment attenuated synapse loss in the brains of AD model mice and inhibited Fe-induced APP cleavage [78,163]. DFO and other Fe chelators are focused on possible treatments for PD [164,165]. Moreover, clioquinol reportedly recovers the memory impairment in scrapie [166], and a Cu 2+ -specific chelator (D-(-)-penicillamine) reportedly inhibits the pathogenesis of prion diseases in vivo [167].…”
Section: Hypothesis: Cross-talk Occurs Between Trace Elements and Amy...mentioning
confidence: 99%