Evidence map›Paper›PMID 27009107›Full record

ArticleCurrent molecular medicine2016

STAT3 Activation in Circulating Monocytes Contributes to Neovascular Age-Related Macular Degeneration.

M Chen, J Lechner, J Zhao, L Toth, R Hogg, G Silvestri, A Kissenpfennig, U Chakravarthy, H Xu

Open access · greenAbstract read
In one paragraph

Article in Current molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.3field-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

39 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. TREM2-Mediated Myeloid Cells Protect Against Pathological Choroidal Neovascularization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Monocytes in Retinal Degeneration: Little Cells with a Big Impact.Advances in experimental medicine and biology · 2025
    Review
  8. Article
  9. Article
  10. Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Immune Cells in Subretinal Wound Healing and Fibrosis.Frontiers in cellular neuroscience · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Deletion of Socs3 in LysMMolecular neurodegeneration · 2021
    Article
  20. Article
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

9 authors at 1 institution in 1 country.

M ChenWellcome-Wolfson Institute of Experimental Medicine, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, UK. m.chen@qub.ac.uk.
J Lechner
J Zhao
L Toth
R Hogg
G Silvestri
A Kissenpfennig
U Chakravarthy
H XuWellcome-Wolfson Institute of Experimental Medicine, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, UK. heping.xu@qub.ac.uk.
Queen's University Belfast · GB

Funding

Medical Research Council G1001795The Dunhill Medical Trust R188/0211
6 · The paper itself

Abstract

Infiltrating macrophages are critically involved in pathogenic angiogenesis such as neovascular agerelated macular degeneration (nAMD). Macrophages originate from circulating monocytes and three subtypes of monocyte exist in humans: classical (CD14(+)CD16(-)), non-classical (CD14(-)CD16(+)) and intermediate (CD14(+)CD16(+)) monocytes. The aim of this study was to investigate the role of circulating monocyte in neovascular age-related macular degeneration (nAMD). Flow cytometry analysis showed that the intermediate monocytes from nAMD patients expressed higher levels of CX3CR1 and HLA-DR compared to those from controls. Monocytes from nAMD patients expressed higher levels of phosphorylated Signal Transducer and Activator of Transcription 3 (pSTAT3), and produced higher amount of VEGF. In the mouse model of choroidal neovascularization (CNV), pSTAT3 expression was increased in the retina and RPE/choroid, and 49.24% of infiltrating macrophages express pSTAT3. Genetic deletion of the Suppressor of Cytokine Signalling 3 (SOCS3) in myeloid cells in the LysM-Cre(+/-):SOCS3(fl/fl) mice resulted in spontaneous STAT3 activation and accelerated CNV formation. Inhibition of STAT3 activation using a small peptide LLL12 suppressed laserinduced CNV. Our results suggest that monocytes, in particular the intermediate subset of monocytes are activated in nAMD patients. STAT3 activation in circulating monocytes may contribute to the development of choroidal neovascularisation in AMD.

Indexed as

AnimalsAnthraquinonesBlotting, WesternCase-Control StudiesChoroidal NeovascularizationHLA-DR AntigensHumansLasersMice, Inbred C57BLMice, KnockoutMiddle AgedMonocytesPhenotypePhosphorylationReceptors, ChemokineRetinaAnthraquinonesHLA-DR AntigensLLL12 compoundReceptors, ChemokineSocs3 protein, mouseSTAT3 Transcription FactorSulfonamidesSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID27009107
PMCPMC4839497
OpenAlexW2305169420

What OpenQuestion holds

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LicenceCC BY-NC
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.