Evidence map›Paper›PMID 30126455›Full record

ArticleMolecular neurodegeneration2018

Subretinal macrophages produce classical complement activator C1q leading to the progression of focal retinal degeneration.

Haihan Jiao, Matt Rutar, Nilisha Fernando, Ted Yednock, Sethu Sankaranarayanan, Riemke Aggio-Bruce, Jan Provis, Riccardo Natoli

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Complement in brain and eye disease: shared mechanisms, convergent pathologies, and common therapeutic opportunities.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Macrophages and Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2025
    Review
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  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

8 authors at 2 institutions in 2 countries.

Haihan JiaoThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia.
Matt RutarThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia.
Nilisha FernandoThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia.
Ted YednockAnnexon Biosciences, South San Francisco, CA, USA.
Sethu SankaranarayananAnnexon Biosciences, South San Francisco, CA, USA.
Riemke Aggio-BruceThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia.
Jan ProvisThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia.
Riccardo NatoliThe John Curtin School of Medical Research, The Australian National University, Building 131, Garran Rd, Canberra, ACT, 2601, Australia. riccardo.natoli@anu.edu.au.ORCID 0000-0002-9350-0439
Australian National University · AUAnnexon Biosciences (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of the alternative complement pathway and its mediation by retinal microglia and macrophages, is well-established in the pathogenesis of Age-Related Macular Degeneration (AMD). However, the contribution of the classical complement pathway towards the progression of retinal degenerations is not fully understood, including the role of complement component 1q (C1q) as a critical activator molecule of the classical pathway. Here, we investigated the contribution of C1q to progressive photoreceptor loss and neuroinflammation in retinal degenerations.

methodsWild-type (WT), C1qa knockout (C1qa

resultsPD mice had increased levels of C1qa which correlated with increasing photoreceptor cell death and macrophage recruitment. C1qa

conclusionsOur data implicate subretinal macrophages, C1q and the classical pathway in progressive retinal degeneration. We demonstrate a role of local C1q produced by microglia/macrophages as an instigator of inflammasome activation and inflammation. Crucially, we have shown that retinal C1q neutralisation during disease progression may slow retinal atrophy, providing a novel strategy for the treatment of complement-mediated retinal degenerations including AMD.

Indexed as

AnimalsComplement C1qDisease ProgressionHumansMacrophagesMiceMice, Inbred C57BLMice, KnockoutRetinal DegenerationComplement C1qAge-related macular degenerationC1qClassical pathwayComplement systemInflammasomeInflammationMacrophagesMicrogliaPhoto-oxidative damageRetinal degeneration

Identifiers

PMID30126455
PMCPMC6102844
OpenAlexW2888519192

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.