Evidence map›Paper›PMID 39468551›Full record

ArticleJournal of neuroinflammation2024

Ganglion cell-derived LysoPS induces retinal neovascularisation by activating the microglial GPR34-PI3K-AKT-NINJ1 axis.

Lushu Chen, HuiYing Zhang, Ying Zhang, Xiumiao Li, MeiHuan Wang, Yaming Shen, Yuan Cao, Yong Xu, Jin Yao

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Microglial polarization in retinal neovascularization: Friend or foe?Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  5. The role of NINJ1 in diseases.Cell death discovery · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Single-cell analysis identifies MKI67Journal of translational medicine · 2025
    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.

Lushu ChenThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
HuiYing ZhangThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
Ying ZhangThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
Xiumiao LiThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
MeiHuan WangThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
Yaming ShenThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China.
Yuan CaoThe Fourth School of Clinical Medicine, Nanjing Medical University, 140 Hanzhong Road, Nanjing, 210029, P. R. China.
Yong XuThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China. yxu4696@njmu.edu.cn.
Jin YaoThe Affiliated Eye Hospital, Nanjing Medical University, 138 Hanzhong Road, Nanjing, 210029, P. R. China. dryaojin@126.com.

Funding

National Natural Science Foundation of China Research Grants Nos. 82271107
6 · The paper itself

Abstract

Retinal neovascularisation is a major cause of blindness in patients with proliferative diabetic retinopathy (PDR). It is mediated by the complex interaction between dysfunctional ganglion cells, microglia, and vascular endothelial cells. Notably, retinal microglia, the intrinsic immune cells of the retina, play a crucial role in the pathogenesis of retinopathy. In this study, we found that lysophosphatidylserines (LysoPS) released from injured ganglion cells induced microglial extracellular trap formation and retinal neovascularisation. Mechanistically, LysoPS activated the GPR34-PI3K-AKT-NINJ1 signalling axis by interacting with the GPR34 receptor on the microglia. This activation upregulated the expression of inflammatory cytokines, such as IL-6, IL-8, VEGFA, and FGF2, and facilitated retinal vascular endothelial cell angiogenesis. As a result, inhibition of the GPR34-PI3K-AKT-NINJ1 axis significantly decreased microglial extracellular trap formation and neovascularisation by suppressing LysoPS-induced microglial inflammatory responses, both in vitro and in vivo. This study reveals the crucial role of apoptotic ganglion cells in activating microglial inflammation in PDR, thereby enhancing our understanding of the pathogenesis of retinal neovascularisation.

Indexed as

MicrogliaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRetinal Ganglion CellsRetinal NeovascularizationSignal TransductionAnimalsHumansLysophospholipidsMaleMiceMice, Inbred C57BLNerve Growth FactorsLysophospholipidsNerve Growth FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktGPR34LysoPSMicroglial extracellular trapsNINJ1PI3K-AKTRetinal neovascularisation

Identifiers

PMID39468551
PMCPMC11520652

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.