Evidence map›Paper›PMID 41199082›Full record

ArticleJournal of molecular neuroscience : MN2025

Microglial Necroptosis Mediated by RIPK3 Leads to Retinal Ganglion Cell Apoptosis Through the Release of FGF2 After Ischemia/Reperfusion.

Jian Liu, Anping Ma, Guangyi Huang, Wen Hu, Xin Xu, Rong Huang, Yaguang Hu, Qiaochu Cheng, Yanlin Feng, Dan Ye and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Jian Liu *Department of Ophthalmology, Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Anping Ma *Department of Ophthalmology, Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Guangyi Huang *Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology &Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences State Key, Nanning, Guangxi, China.
Wen Hu *Department of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology &Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences State Key, Nanning, Guangxi, China.
Xin Xu *Medical School, Nantong University, Nantong, Jiangsu, China.
Rong HuangDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Yaguang HuDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Qiaochu ChengDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yanlin FengState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen University, Guangzhou, China.
Dan YeState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-Sen University, Guangzhou, China.
Fan XuDepartment of Ophthalmology, the People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology &Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences State Key, Nanning, Guangxi, China.
Aimin SangDepartment of Ophthalmology, Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China. sangam@ntu.edu.cn.

Funding

the Guangzhou Science and Technology Bureau Basic Research Program 2025A03J4483the National Natural Science Foundation of China 82201214the National Natural Science Foundation of China 82201221the National Natural Science Foundation of China 82401253the National Natural Science Foundation of China 82401285the project of Research and Development of New Technologies and Systems for Low Vision Rehabilitation at Nantong University School of Medicine 23ZH313
6 · The paper itself

Abstract

The aim of this study was to explore the function of receptor-interacting protein kinase 3 (RIPK3) on retinal neuron damage induced by retinal ischemia/reperfusion (IR). Microglia-specific RIPK3 knockout (KO) mice were employed to establish retinal IR models. Retinal structural and functional status was assessed using hematoxylin and eosin staining along with electroretinogram. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was employed to detect the situations of apoptotic cell death. Immunofluorescence and western blot were applied to detect the proteins associated with necroptosis and retinal inner neurons. Following retinal IR, necroptosis-related protein RIPK3 became activated within microglia, inducing the activation of mixed lineage kinase domain-like protein (MLKL). RIPK3 KO significantly alleviated IR-induced retinal morphological defects and protected against IR-induced visual dysfunction by preserving neurons within the retina. Additionally, the counts of TUNEL

Indexed as

ApoptosisFibroblast Growth Factor 2MicrogliaNecroptosisReceptor-Interacting Protein Serine-Threonine KinasesReperfusion InjuryRetinal Ganglion CellsAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutProtein KinasesFibroblast Growth Factor 2MLKL protein, mouseProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseIschemia/reperfusionNecroptosisNeuronal injuryRetinal ganglion cellsRIPK3

Identifiers

PMID41199082

What Socratic holds

Textmetadata
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.