Evidence map›Paper›PMID 42533588›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026

Ninjurin2 Promotes Pulmonary Endothelial Barrier Dysfunction Through VEGF/VEGFR2 Signaling Pathway.

Huixin Peng, Yubing Yu, Liujinhong Han, Yuan He, Pengyun Wang, Jiahui Zhuo, Chengqi Xu, Huiying Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Huixin PengShandong Provincial Lab for Clinical Immunology Translational Medicine in Universities, First Affiliated Hospital of Shandong First Medical University/Shandong Province Qianfoshan Hospital, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, P. R. China.
Yubing YuInstitute of Medical Genomics, Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, NHC Key Laboratory of Biotechnology Drugs (Shandong Academy of Medical Sciences), First Affiliated Hospital of Shandong First Medical University/Shandong Province Qianfoshan Hospital, Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, P. R. China.
Liujinhong HanCollege of Pulmonary and Critical Care Medicine, the 8th Medical Centre, Chinese PLA General Hospital, Beijing, P. R. China.
Yuan HeCollege of Pulmonary and Critical Care Medicine, the 8th Medical Centre, Chinese PLA General Hospital, Beijing, P. R. China.
Pengyun WangDepartment of Clinical Laboratory, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P. R. China.
Jiahui ZhuoCenter for Human Genome Research, Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China.
Chengqi XuCenter for Human Genome Research, Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China.
Huiying LiuCollege of Pulmonary and Critical Care Medicine, the 8th Medical Centre, Chinese PLA General Hospital, Beijing, P. R. China.ORCID https://orcid.org/0000-0001-5281-8064

Funding

Beijing Natural Science Foundation of China 7242132Beijing Natural Science Foundation of China L232125National Natural Science Foundation of Hubei Province 2023AFB848the National Natural Science Foundation of China 32470640the National Natural Science Foundation of China 82170087
6 · The paper itself

Abstract

Previous studies have established an association between Ninjurin2 and diseases related to vascular endothelial dysfunction, such as ischemic stroke and coronary heart disease. Given that impaired pulmonary endothelial barrier function is a critical feature of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), we hypothesized that Ninjurin2 may also participate in the regulation of lung vascular permeability. Therefore, this study investigates the role of Ninjurin2 in regulating endothelial cell function and dysfunction, aiming to elucidate the underlying mechanisms in ALI and ARDS. This study utilized both animal models and in vitro experiments to investigate the role of Ninjurin2 in regulating endothelial cell function and dysfunction. Endothelial-specific Ninjurin2 overexpressing (NINJ2-TG

Indexed as

Cell Adhesion Molecules, NeuronalEndothelial CellsEndothelium, VascularLungNerve Growth FactorsSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Acute Lung InjuryAnimalsCapillary PermeabilityHumansMaleMiceMice, Inbred C57BLCell Adhesion Molecules, NeuronalKdr protein, mouseNerve Growth FactorsNinj1 protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-2ALIARDSendothelial cell function and dysfunctionNinjurin2VEGF/VEGFR2

Identifiers

PMID42533588
PMCPMC13425037

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.