Evidence map›Paper›PMID 23608111›Full record

ArticleNeurobiology of aging2013

Gene expression changes in aging retinal microglia: relationship to microglial support functions and regulation of activation.

Wenxin Ma, Radu Cojocaru, Norimoto Gotoh, Linn Gieser, Rafael Villasmil, Tiziana Cogliati, Anand Swaroop, Wai T Wong

Abstract read
In one paragraph

Article in Neurobiology of aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The Role of Complement Dysregulation in Glaucoma.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Functional genomics of inflamm-aging and immunosenescence.Briefings in functional genomics · 2022
    Review
  19. Immune Cells in Subretinal Wound Healing and Fibrosis.Frontiers in cellular neuroscience · 2022
    Review
  20. Article

1 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

8 authors at 1 institution in 1 country.

Wenxin MaUnit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Radu Cojocaru
Norimoto Gotoh
Linn Gieser
Rafael Villasmil
Tiziana Cogliati
Anand Swaroop
Wai T Wong
National Institutes of Health · US

Funding

Retinal aging and inherited neurodegenerative diseasesZIAEY000473 · NEI · NATIONAL EYE INSTITUTE · PI SWAROOP, ANAND · 2009 to 2014
$16.2M
Dynamic Imaging of Retinal MicrogliaZIAEY000463 · NEI · NATIONAL EYE INSTITUTE · PI WONG, WAI · 2009 to 2020
$7.3M
Flow Cytometry COREZICEY000457 · NEI · NATIONAL EYE INSTITUTE · PI CASPI, RACHEL R. · 2009 to 2025
$5.9M
Intramural NIH HHS ZIA EY000463
6 · The paper itself

Abstract

Microglia, the resident immune cells of the central nervous system (CNS), are thought to contribute to the pathogenesis of age-related neurodegenerative disorders. It has been hypothesized that microglia undergo age-related changes in gene expression patterns that give rise to pathogenic phenotypes. We compared the gene expression profiles in microglia isolated ex vivo from the retinas of mice ranging from early adulthood to late senescence. We discovered that microglial gene expression demonstrated progressive change with increasing age, and involved genes that regulate microglial supportive functions and immune activation. Molecular pathways involving immune function and regulation, angiogenesis, and neurotrophin signaling demonstrated age-related change. In particular, expression levels of complement genes, C3 and CFB, previously associated with age-related macular degeneration (AMD), increased with aging, suggesting that senescent microglia may contribute to complement dysregulation during disease pathogenesis. Taken together, senescent microglia demonstrate age-related gene expression changes capable of altering their constitutive support functions and regulation of their activation status in ways relating to neuroinflammation and neurodegeneration in the CNS.

Indexed as

Gene Expression Regulation, DevelopmentalAgingAnimalsCentral Nervous System DiseasesComplement C3cComplement Factor BGene Expression ProfilingImmunityInflammationMacular DegenerationMaleMiceMice, Inbred C57BLMicrogliaNerve Growth FactorsNeurodegenerative DiseasesComplement C3cComplement Factor BNerve Growth FactorsActivationAgingAngiogenesisComplementGene expressionMicroarrayMicrogliaNeurotrophic factorsRetinaSenescence

Identifiers

PMID23608111
PMCPMC3706521
OpenAlexW1991747977

What OpenQuestion holds

Textmetadata
LicenceTDM
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.