Evidence map›Paper›PMID 37240109›Full record

ReviewInternational journal of molecular sciences2023

Dysfunctional Autophagy, Proteostasis, and Mitochondria as a Prelude to Age-Related Macular Degeneration.

Raji Rajesh Lenin, Yi Hui Koh, Zheting Zhang, Yan Zhuang Yeo, Bhav Harshad Parikh, Ivan Seah, Wendy Wong, Xinyi Su

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 23 citations in OpenAlex.

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  19. Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Raji Rajesh LeninDepartment of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.ORCID 0009-0002-3774-0259
Yi Hui KohDepartment of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.ORCID 0009-0005-7482-5835
Zheting ZhangDepartment of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.ORCID 0009-0004-0797-8439
Yan Zhuang YeoInstitute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), 61 Biopolis Drive, Proteos, Singapore 138673, Singapore.
Bhav Harshad ParikhInstitute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), 61 Biopolis Drive, Proteos, Singapore 138673, Singapore.ORCID 0000-0003-3835-8887
Ivan SeahDepartment of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.ORCID 0000-0001-7843-1917
Wendy WongDepartment of Ophthalmology, National University Hospital (NUH), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.
Xinyi SuDepartment of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), 1E Kent Ridge Road, NUHS Tower Block Level 7, Singapore 119228, Singapore.
Agency for Science, Technology and Research · SGNational University of Singapore · SGNational University Hospital · SGSRM Institute of Science and Technology · IN

Funding

Ministry of Education MOET32020-0001
6 · The paper itself

Abstract

Retinal pigment epithelial (RPE) cell dysfunction is a key driving force of AMD. RPE cells form a metabolic interface between photoreceptors and choriocapillaris, performing essential functions for retinal homeostasis. Through their multiple functions, RPE cells are constantly exposed to oxidative stress, which leads to the accumulation of damaged proteins, lipids, nucleic acids, and cellular organelles, including mitochondria. As miniature chemical engines of the cell, self-replicating mitochondria are heavily implicated in the aging process through a variety of mechanisms. In the eye, mitochondrial dysfunction is strongly associated with several diseases, including age-related macular degeneration (AMD), which is a leading cause of irreversible vision loss in millions of people globally. Aged mitochondria exhibit decreased rates of oxidative phosphorylation, increased reactive oxygen species (ROS) generation, and increased numbers of mitochondrial DNA mutations. Mitochondrial bioenergetics and autophagy decline during aging because of insufficient free radical scavenger systems, the impairment of DNA repair mechanisms, and reductions in mitochondrial turnover. Recent research has uncovered a much more complex role of mitochondrial function and cytosolic protein translation and proteostasis in AMD pathogenesis. The coupling of autophagy and mitochondrial apoptosis modulates the proteostasis and aging processes. This review aims to summarise and provide a perspective on (i) the current evidence of autophagy, proteostasis, and mitochondrial dysfunction in dry AMD; (ii) current in vitro and in vivo disease models relevant to assessing mitochondrial dysfunction in AMD, and their utility in drug screening; and (iii) ongoing clinical trials targeting mitochondrial dysfunction for AMD therapeutics.

Indexed as

Macular DegenerationRetinal Pigment EpitheliumAgedAutophagyHumansMitochondriaOxidative StressProteostasisage-related macular degenerationagingautophagyclinical trialsmitochondrial dysfunctionretinal pigment epithelium

Identifiers

PMID37240109
PMCPMC10217992
OpenAlexW4378516733

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.