Article in Nature communications, 2026. 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.
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.
Mu Yang *Genetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0000-0002-6001-6827
Rulian Zhao *Department of Ophthalmology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.
Li Peng *Genetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0000-0002-7041-9267
Liting Lv *Genetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0009-0001-0928-077X
Lanyao YangGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0009-0006-5500-3892
Yunqi HeGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0000-0002-5265-3244
Xu HaGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0009-0007-5430-2919
Huijuan XuGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.ORCID http://orcid.org/0000-0002-1858-1822
Xiang ZhangDepartment of Ophthalmology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.ORCID http://orcid.org/0000-0002-1277-4615
Peiquan ZhaoDepartment of Ophthalmology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.ORCID http://orcid.org/0000-0002-5092-9550
Shujin LiGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China. lishujin91@126.com.ORCID http://orcid.org/0000-0002-7691-3776
Zhenglin YangGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China. yangzhenglin@cashq.ac.cn.ORCID http://orcid.org/0000-0002-8656-7862
Funding
China Postdoctoral Science Foundation 2023M740518China Postdoctoral Science Foundation 2024M750365Department of Science and Technology of Sichuan Province (Sichuan Provincial Department of Science and Technology) 2023ZYD0172National Natural Science Foundation of China (National Science Foundation of China) 82121003National Natural Science Foundation of China (National Science Foundation of China) 82301231National Natural Science Foundation of China (National Science Foundation of China) 82401292National Natural Science Foundation of China (National Science Foundation of China) 82471102National Natural Science Foundation of China (National Science Foundation of China) 82501315National Natural Science Foundation of China (National Science Foundation of China) 82571242National Natural Science Foundation of China (National Science Foundation of China) U25A6002
6 · The paper itself
Abstract
Familial exudative vitreoretinopathy is a hereditary disorder predominantly affecting infants and young children, often leading to severe vision loss. Approximately 40% of patients carry mutations in Norrin/β-catenin pathway genes. Nevertheless, the downstream pathogenic mechanisms remain unclear. Here, by using bulk RNA sequencing and single-cell RNA sequencing analyses, we identify KIF11 as a key downstream effector in retinal endothelial cells. Lentivirus-mediated KIF11 overexpression partially restores vascular defects in endothelial cell-specific Ctnnb1 knockout mice. Functional and multi-omics studies reveal that β-catenin/KIF11 deficiency induces autophagy-accompanied ferroptosis. Mechanistically, KIF11 binds PRDX1, and the disrupted β-catenin/KIF11 axis releases the competitive restraint of KIF11 on Src-mediated PRDX1 phosphorylation, triggering subsequent liquid-liquid phase separation. Treatment with the ferroptosis inhibitor ferrostatin-1 or lentiviral overexpression of non-phosphorylatable PRDX1 partially rescues vascular defects in familial exudative vitreoretinopathy-associated mice. Overall, we elucidate a β-catenin/KIF11/PRDX1 axis-dependent ferroptosis mechanism in familial exudative vitreoretinopathy, highlighting ferroptosis-targeting and antioxidant strategies as potential therapies.
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.
KIF11 prevents retinal endothelial ferroptosis in familial exudative vitreoretinopathy by inhibiting phosphorylation-driven PRDX1 phase separation. · full record | Socratic