Evidence map›Paper›PMID 37222160›Full record

ArticleMolecules and cells2023

The Bcl-2/Bcl-xL Inhibitor ABT-263 Attenuates Retinal Degeneration by Selectively Inducing Apoptosis in Senescent Retinal Pigment Epithelial Cells.

Wonseon Ryu, Chul-Woo Park, Junghoon Kim, Hyungwoo Lee, Hyewon Chung

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
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  6. From environmental exposure to retinal pathology: epidemiological and mechanistic insights into multi-metal driven ocular diseases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  7. Review
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  13. Diabetic macular edema: Upcoming therapies.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Review
  14. Article
  15. Article
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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 1 institution in 1 country.

Wonseon RyuDepartment of Ophthalmology, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID https://orcid.org/0000-0001-5604-1803
Chul-Woo ParkDepartment of Ophthalmology, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID https://orcid.org/0000-0003-1471-8366
Junghoon KimDepartment of Ophthalmology, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID https://orcid.org/0000-0002-9517-9087
Hyungwoo LeeDepartment of Ophthalmology, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID https://orcid.org/0000-0002-3248-4754
Hyewon ChungDepartment of Ophthalmology, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID https://orcid.org/0000-0003-1312-6406
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is one of the leading causes of blindness in elderly individuals. However, the currently used intravitreal injections of anti-vascular endothelial growth factor are invasive, and repetitive injections are also accompanied by a risk of intraocular infection. The pathogenic mechanism of AMD is still not completely understood, but a multifactorial mechanism that combines genetic predisposition and environmental factors, including cellular senescence, has been suggested. Cellular senescence refers to the accumulation of cells that stop dividing due to the presence of free radicals and DNA damage. Characteristics of senescent cells include nuclear hypertrophy, increased levels of cell cycle inhibitors such as p16 and p21, and resistance to apoptosis. Senolytic drugs remove senescent cells by targeting the main characteristics of these cells. One of the senolytic drugs, ABT-263, which inhibits the antiapoptotic functions of Bcl-2 and Bcl-xL, may be a new treatment for AMD patients because it targets senescent retinal pigment epithelium (RPE) cells. We proved that it selectively kills doxorubicin (Dox)-induced senescent ARPE-19 cells by activating apoptosis. By removing senescent cells, the expression of inflammatory cytokines was reduced, and the proliferation of the remaining cells was increased. When ABT-263 was orally administered to the mouse model of senescent RPE cells induced by Dox, we confirmed that senescent RPE cells were selectively removed and retinal degeneration was alleviated. Therefore, we suggest that ABT-263, which removes senescent RPE cells through its senolytic effect, has the potential to be the first orally administered senolytic drug for the treatment of AMD.

Indexed as

Antineoplastic AgentsMacular DegenerationRetinal DegenerationAniline CompoundsAnimalsApoptosisCellular SenescenceEpithelial CellsMiceRetinal PigmentsSenotherapeuticsSulfonamidesAniline CompoundsAntineoplastic AgentsnavitoclaxRetinal PigmentsSenotherapeuticsSulfonamidesABT-263Bcl-2/Bcl-xLdoxorubicinsenescencesenolytic

Identifiers

PMID37222160
PMCPMC10336274
OpenAlexW4377939820

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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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.