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Article: Novel Programmed Cell Death as Therapeutic Targets in Age-Related Macular Degeneration?

TitleNovel Programmed Cell Death as Therapeutic Targets in Age-Related Macular Degeneration?
Authors
Keywordsretina
vision
ocular stress
cell damage
homeostasis
Issue Date2020
PublisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms
Citation
International Journal of Molecular Sciences, 2020, v. 21 n. 19, p. article no. 7279 How to Cite?
AbstractAge-related macular degeneration (AMD) is a leading cause of severe visual loss among the elderly. AMD patients are tormented by progressive central blurring/loss of vision and have limited therapeutic options to date. Drusen accumulation causing retinal pigment epithelial (RPE) cell damage is the hallmark of AMD pathogenesis, in which oxidative stress and inflammation are the well-known molecular mechanisms. However, the underlying mechanisms of how RPE responds when exposed to drusen are still poorly understood. Programmed cell death (PCD) plays an important role in cellular responses to stress and the regulation of homeostasis and diseases. Apart from the classical apoptosis, recent studies also discovered novel PCD pathways such as pyroptosis, necroptosis, and ferroptosis, which may contribute to RPE cell death in AMD. This evidence may yield new treatment targets for AMD. In this review, we summarized and analyzed recent advances on the association between novel PCD and AMD, proposing PCD’s role as a therapeutic new target for future AMD treatment.
Persistent Identifierhttp://hdl.handle.net/10722/289575
ISSN
2011 Impact Factor: 2.598
2020 SCImago Journal Rankings: 1.455
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYANG, M-
dc.contributor.authorSo, KF-
dc.contributor.authorLam, WC-
dc.contributor.authorLo, ACY-
dc.date.accessioned2020-10-22T08:14:34Z-
dc.date.available2020-10-22T08:14:34Z-
dc.date.issued2020-
dc.identifier.citationInternational Journal of Molecular Sciences, 2020, v. 21 n. 19, p. article no. 7279-
dc.identifier.issn1661-6596-
dc.identifier.urihttp://hdl.handle.net/10722/289575-
dc.description.abstractAge-related macular degeneration (AMD) is a leading cause of severe visual loss among the elderly. AMD patients are tormented by progressive central blurring/loss of vision and have limited therapeutic options to date. Drusen accumulation causing retinal pigment epithelial (RPE) cell damage is the hallmark of AMD pathogenesis, in which oxidative stress and inflammation are the well-known molecular mechanisms. However, the underlying mechanisms of how RPE responds when exposed to drusen are still poorly understood. Programmed cell death (PCD) plays an important role in cellular responses to stress and the regulation of homeostasis and diseases. Apart from the classical apoptosis, recent studies also discovered novel PCD pathways such as pyroptosis, necroptosis, and ferroptosis, which may contribute to RPE cell death in AMD. This evidence may yield new treatment targets for AMD. In this review, we summarized and analyzed recent advances on the association between novel PCD and AMD, proposing PCD’s role as a therapeutic new target for future AMD treatment.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms-
dc.relation.ispartofInternational Journal of Molecular Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectretina-
dc.subjectvision-
dc.subjectocular stress-
dc.subjectcell damage-
dc.subjecthomeostasis-
dc.titleNovel Programmed Cell Death as Therapeutic Targets in Age-Related Macular Degeneration?-
dc.typeArticle-
dc.identifier.emailSo, KF: hrmaskf@hku.hk-
dc.identifier.emailLam, WC: waichlam@hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.authoritySo, KF=rp00329-
dc.identifier.authorityLam, WC=rp02162-
dc.identifier.authorityLo, ACY=rp00425-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/ijms21197279-
dc.identifier.pmid33019767-
dc.identifier.pmcidPMC7582463-
dc.identifier.scopuseid_2-s2.0-85091891495-
dc.identifier.hkuros316954-
dc.identifier.volume21-
dc.identifier.issue19-
dc.identifier.spagearticle no. 7279-
dc.identifier.epagearticle no. 7279-
dc.identifier.isiWOS:000586646400001-
dc.publisher.placeSwitzerland-
dc.identifier.issnl1422-0067-

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