Show simple item record

dc.contributor.authorBoag, Matthew K
dc.contributor.authorMa, Linlin
dc.contributor.authorMellick, George D
dc.contributor.authorPountney, Dean L
dc.contributor.authorFeng, Yunjiang
dc.contributor.authorQuinn, Ronald J
dc.contributor.authorLiew, Alan Wee-Chung
dc.contributor.authorDharmasivam, Mahendiran
dc.contributor.authorAzad, Mahan Gholam
dc.contributor.authorAfroz, Rizwana
dc.contributor.authorRichardson, Des R
dc.date.accessioned2021-10-13T04:22:27Z
dc.date.available2021-10-13T04:22:27Z
dc.date.issued2021
dc.identifier.issn2213-2317
dc.identifier.doi10.1016/j.redox.2021.102136
dc.identifier.urihttp://hdl.handle.net/10072/409000
dc.description.abstractAutonomously spiking dopaminergic neurons of the substantia nigra pars compacta (SNpc) are exquisitely specialized and suffer toxic iron-loading in Parkinson's disease (PD). However, the molecular mechanism involved remains unclear and critical to decipher for designing new PD therapeutics. The long-lasting (L-type) CaV1.3 voltage-gated calcium channel is expressed at high levels amongst nigral neurons of the SNpc, and due to its role in calcium and iron influx, could play a role in the pathogenesis of PD. Neuronal iron uptake via this route could be unregulated under the pathological setting of PD and potentiate cellular stress due to its redox activity. This Commentary will focus on the role of the CaV1.3 channels in calcium and iron uptake in the context of pharmacological targeting. Prospectively, the audacious use of artificial intelligence to design innovative CaV1.3 channel inhibitors could lead to breakthrough pharmaceuticals that attenuate calcium and iron entry to ameliorate PD pathology.
dc.description.peerreviewedYes
dc.languageen
dc.publisherElsevier BV
dc.relation.ispartofpagefrom102136
dc.relation.ispartofjournalRedox Biology
dc.relation.ispartofvolume47
dc.subject.fieldofresearchNeurology and neuromuscular diseases
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences
dc.subject.fieldofresearchBiochemistry and cell biology
dc.subject.fieldofresearchMedical biochemistry and metabolomics
dc.subject.fieldofresearchMedicinal and biomolecular chemistry
dc.subject.fieldofresearchcode320905
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3214
dc.subject.fieldofresearchcode3101
dc.subject.fieldofresearchcode3205
dc.subject.fieldofresearchcode3404
dc.titleCalcium channels and iron metabolism: A redox catastrophe in Parkinson's disease and an innovative path to novel therapies?
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationBoag, MK; Ma, L; Mellick, GD; Pountney, DL; Feng, Y; Quinn, RJ; Liew, AW-C; Dharmasivam, M; Azad, MG; Afroz, R; Richardson, DR, Calcium channels and iron metabolism: A redox catastrophe in Parkinson's disease and an innovative path to novel therapies?, Redox Biology, 2021, 47, pp. 102136
dcterms.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.date.updated2021-09-24T03:06:16Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2021 The Authors.Published by Elsevier B.V. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International (CC BY-NC-ND 4.0) License, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorFeng, Yun J.
gro.griffith.authorRichardson, Des R.
gro.griffith.authorLiew, Alan Wee-Chung
gro.griffith.authorMa, Linlin
gro.griffith.authorMellick, George
gro.griffith.authorPountney, Dean L.
gro.griffith.authorQuinn, Ronald J.
gro.griffith.authorDharmasivam, Mahendiran
gro.griffith.authorAfroz, Rizwana


Files in this item

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record