Evidence map›Paper›PMID 42469820›Full record

ArticleJournal of neuroinflammation2026

CCR1 signaling as a common injury pathway in retinal degeneration.

Sarah Elbaz-Hayoun, Lian Omari, Shlomit Jaskoll, Adi Kramer, Batya Rinsky, Maya Eiger-Moscovich, Ying Song, Joshua L Dunaief, Sandro De Zanet, Stefanos Apostolopoulos and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Sarah Elbaz-HayounDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Lian OmariDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Shlomit JaskollDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Adi KramerDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Batya RinskyDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Maya Eiger-MoscovichDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel.
Ying SongFM Kirby Center for Molecular Ophthalmology, Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Joshua L DunaiefFM Kirby Center for Molecular Ophthalmology, Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Sandro De ZanetRetinAI Medical AG, Freiburgstrasse 3, Bern, CH-3010, Switzerland.
Stefanos ApostolopoulosRetinAI Medical AG, Freiburgstrasse 3, Bern, CH-3010, Switzerland.
Carlos CillerRetinAI Medical AG, Freiburgstrasse 3, Bern, CH-3010, Switzerland.
Itay ChowersDepartment of Ophthalmology, Hadassah-Hebrew University Medical Center, and the Hebrew University - Hadassah School of Medicine, POB 12000, Jerusalem, 91120, Israel. chowers@hadassah.org.il.

Funding

Israel Science Foundation 2080/23the Israeli Ministry of Science 0007972
6 · The paper itself

Abstract

Inflammation is a key driver of atrophic Age-Related Macular Degeneration (aAMD), and also plays a role in Inherited Retinal Degenerations (IRDs), two major causes of irreversible visual loss. We previously demonstrated that the C-C chemokine receptor type 1 (CCR1) is upregulated in monocytes from AMD patients, and that it mediates the recruitment of neurotoxic macrophages and activates Müller glial cells in rodent model of photic retinal injury. Here we report that CCR1 is expressed in Müller glia in eyes affected by AMD and that variants in CCR1 are potentially associated with the rate of macular atrophy progression in AMD. We also show that Ccr1 deletion is associated with reduced inflammation, and with rescue of photoreceptor integrity and function in Crb1

Indexed as

Receptors, CCR1Retinal DegenerationSignal TransductionAnimalsDisease Models, AnimalEpendymoglial CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicCcr1 protein, mouseReceptors, CCR1C-C chemokine receptor type 1 (CCR1)Ccr1 deletionCCR1 inhibitionGliosisMicroglial activationMüller cellRd10 mutationRd8 mutationRetinal degenerationSmall molecule

Identifiers

PMID42469820
PMCPMC13670453

What OpenQuestion holds

Textmetadata
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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.