Evidence map›Paper›PMID 40611130›Full record

ArticleJournal of neuroinflammation2025

Factor-H-related protein 1 (FHR1), a promotor of para-inflammation in age-related macular degeneration.

Andjela Sekulic, Sarah M Herr, Kelly Mulfaul, Inga-Marie Pompös, Silvia Winkler, Carola Dietrich, Benedikt Obermayer, Robert F Mullins, Thomas Conrad, Peter F Zipfel and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

13 authors.

Andjela SekulicExperimental Ophthalmology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.
Sarah M HerrInstitute of Cell Biochemistry, Hannover Medical School, 30625, Hannover, Germany.
Kelly MulfaulDepartment of Neuroscience and Pharmacology, University of Iowa, Iowa City, USA.
Inga-Marie PompösExperimental Ophthalmology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.
Silvia WinklerExperimental Ophthalmology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany.
Carola DietrichGenomics Technology Platform, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Benedikt ObermayerCore Unit Bioinformatics, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Robert F MullinsInstitute for Vision Research, Department of Ophthalmology & Visual Sciences, University of Iowa, Iowa City, USA.
Thomas ConradGenomics Technology Platform, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Peter F ZipfelFaculty of Biosciences, Friedrich Schiller University, 07743, Jena, Germany.
Florian SennlaubSorbonne University, INSERM, CNRS, Institut de la Vision, 17 rue Moreau, Paris, F-75012, France.
Christine SkerkaDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, 07745, Jena, Germany. christine.skerka@googlemail.com.
Olaf StraußExperimental Ophthalmology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117, Berlin, Germany. olaf.strauss@charite.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD), a multifactorial type of retinal degeneration represents the most common cause for blindness in elderly. Polymorphisms in complement factor-H increase, while absence of factor-H-related protein-1 (FHR1) decreases the AMD risk, currently explained by their opposing relationship. Here we identify a FHR1-driven pathway fostering chronic cellular inflammation. FHR1 accumulates below the retinal pigment epithelium (RPE) in AMD donor tissue and similarly the murine homolog, muFHR1 is abundant in three AMD-relevant mouse models. These mouse models express the muFHR1 receptor EGF-like module-containing mucin-like hormone receptor 1 (Emr1) on the RPE and on invading mononuclear phagocytes (MP), where both cells form clusters via muFHR1/Emr1. FHR1 ignited EMR2-dependent Ca

Indexed as

Complement C3b Inactivator ProteinsInflammationMacular DegenerationAnimalsDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicRetinal Pigment EpitheliumCFHR1 protein, humanComplement C3b Inactivator ProteinsAge-related macular degenerationComplement systemInflammationRetinal pigment epithelium

Identifiers

PMID40611130
PMCPMC12226897

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.