Evidence map›Paper›PMID 33482879›Full record

ReviewJournal of neuroinflammation2021

Cellular senescence in the aging retina and developments of senotherapies for age-related macular degeneration.

Keng Siang Lee, Shuxiao Lin, David A Copland, Andrew D Dick, Jian Liu

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
8.0field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 139 citations in OpenAlex.

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  15. Lack of Pnpla2 Accelerates Progression of AMD-Like Features in Mice.Investigative ophthalmology & visual science · 2025
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27 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Keng Siang Lee *Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol, BS8 1TD, UK.
Shuxiao Lin *School of Cellular and Molecular Medicine, University of Bristol, Bristol, BS8 1TD, UK.
David A CoplandBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, BS8 1TD, UK.
Andrew D DickBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, BS8 1TD, UK. a.dick@bristol.ac.uk.
Jian LiuBristol Medical School, Translational Health Sciences, University of Bristol, Bristol, BS8 1TD, UK. jian.liu@bristol.ac.uk.ORCID http://orcid.org/0000-0002-8600-3979
University of Bristol · GBMoorfields Eye Hospital NHS Foundation Trust · GB

Funding

Rosetrees Trust M418-F1
6 · The paper itself

Abstract

Age-related macular degeneration (AMD), a degenerative disease in the central macula area of the neuroretina and the supporting retinal pigment epithelium, is the most common cause of vision loss in the elderly. Although advances have been made, treatment to prevent the progressive degeneration is lacking. Besides the association of innate immune pathway genes with AMD susceptibility, environmental stress- and cellular senescence-induced alterations in pathways such as metabolic functions and inflammatory responses are also implicated in the pathophysiology of AMD. Cellular senescence is an adaptive cell process in response to noxious stimuli in both mitotic and postmitotic cells, activated by tumor suppressor proteins and prosecuted via an inflammatory secretome. In addition to physiological roles in embryogenesis and tissue regeneration, cellular senescence is augmented with age and contributes to a variety of age-related chronic conditions. Accumulation of senescent cells accompanied by an impairment in the immune-mediated elimination mechanisms results in increased frequency of senescent cells, termed "chronic" senescence. Age-associated senescent cells exhibit abnormal metabolism, increased generation of reactive oxygen species, and a heightened senescence-associated secretory phenotype that nurture a proinflammatory milieu detrimental to neighboring cells. Senescent changes in various retinal and choroidal tissue cells including the retinal pigment epithelium, microglia, neurons, and endothelial cells, contemporaneous with systemic immune aging in both innate and adaptive cells, have emerged as important contributors to the onset and development of AMD. The repertoire of senotherapeutic strategies such as senolytics, senomorphics, cell cycle regulation, and restoring cell homeostasis targeted both at tissue and systemic levels is expanding with the potential to treat a spectrum of age-related diseases, including AMD.

Indexed as

AgingCellular SenescenceMacular DegenerationRetinaAnimalsHumansCellular senescenceImmune agingMacular degenerationMicrogliaNeuronRetinal pigment epitheliumSASP

Identifiers

PMID33482879
PMCPMC7821689
OpenAlexW3123063922

What OpenQuestion 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 OpenQuestion graph.