Evidence map›Paper›PMID 40395179›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Immune Checkpoint PD-L1 Modulates Retinal Microglial Activation to Alleviate Vascular Leakage in Choroidal Neovascularization via ERK.

Yue Zou, Junliang Jiang, Yunqin Li, Xinyi Ding, Qiuping Tong, Ying Shi, Lei Xiao, Ling Chen

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

8 authors.

Yue ZouEye Institute and Department of Ophthalmology, Eye & ENT Hospital, NHC Key Laboratory of Myopia (Fudan University); Key Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Junliang JiangDepartment of Orthopedics & Traumatology, Affiliated Hospital of Yunnan University, Yunnan University, Kunming, 650021, China.
Yunqin LiDepartment of Ophthalmology, Yunnan Eye Institute & Key Laboratory of Yunnan Province, Yunnan Eye Disease Clinical Medical Center, Affiliated Hospital of Yunnan University, Yunnan University, Kunming, 650021, China.
Xinyi DingEye Institute and Department of Ophthalmology, Eye & ENT Hospital, NHC Key Laboratory of Myopia (Fudan University); Key Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.
Qiuping TongThe State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Ying ShiThe State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Lei XiaoThe State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, and the Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Ling ChenEye Institute and Department of Ophthalmology, Eye & ENT Hospital, NHC Key Laboratory of Myopia (Fudan University); Key Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, 200031, China.ORCID https://orcid.org/0000-0003-2430-8432

Funding

National Natural Science Foundation of China 81371042National Natural Science Foundation of China 81870660Science and Technology Innovation Action Plan of Shanghai Science and Technology Commission 22Y11910500Yunnan Provincial Department of Science and Technology - Kunming Medical University Joint Fund for Applied Basic Research 202401AY070001-172/174Yunnan Provincial Young and Middle - Aged Academic and Technical Leaders Reserve Talents Project 202305AC160073
6 · The paper itself

Abstract

Neovascular age-related macular degeneration (NVAMD) is a common retinal disease causing vision loss in the elderly. Neuroinflammation significantly contributes to NVAMD's etiology. This study explores the role of Programmed cell death ligand 1 (PD-L1), an immune checkpoint (ICP) in microglia, known for limiting neuroinflammation in neurodegenerative diseases, and its potential function in NVAMD. This work finds increased PD-L1 expression in retinal microglia following laser injury. PD-L1 knockout (KO) or inhibitory PD-L1 antibody treatment worsens vascular leakage and neoangiogenesis in a laser-induced NVAMD mouse model, effects reversible by microglia depletion with PLX5622. This study underscores that choroidal neovascularization (CNV) may be regulated by multiple mechanisms, with PD-L1 modulation representing one of these pathways. Blocking PD-L1 elevated proinflammatory factors and p-ERK levels, indicating microglial overactivation in NVAMD. Conversely, enhancing PD-L1 signaling reduced neuroinflammation and neovascularization via ERK. These findings highlight PD-L1's role in neoangiogenesis and neuroinflammation in NVAMD, suggesting its potential as a target for immunomodulatory treatment in NVAMD.

Indexed as

B7-H1 AntigenChoroidal NeovascularizationMacular DegenerationMicrogliaRetinaAnimalsDisease Models, AnimalHumansMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutB7-H1 AntigenCd274 protein, mousemicroglia/macrophageneovascular age‐related macular degenerationneuroinflammation, PD‐L1

Identifiers

PMID40395179
PMCPMC12199325

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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.