Evidence map›Paper›PMID 36969192›Full record

ArticleFrontiers in immunology2023

Deficiency of endothelial FGFR1 signaling via upregulation of ROCK2 activity aggravated ALI/ARDS.

Yue Deng, Xingming Huang, Yan Hu, Weiting Zhong, Hua Zhang, Chunheng Mo, Hongjun Wang, Bi-Sen Ding, Chen Wang

Open access · goldFull text read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Ninjurin2 Promotes Pulmonary Endothelial Barrier Dysfunction Through VEGF/VEGFR2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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 at 4 institutions in 1 country.

Yue DengPeking University China-Japan Friendship School of Clinical Medicine, Beijing, China.
Xingming HuangKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
Yan HuKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
Weiting ZhongBeijing Tide Pharmaceutical Co., Ltd., Beijing, China.
Hua ZhangKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
Chunheng MoKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
Hongjun WangBeijing Tide Pharmaceutical Co., Ltd., Beijing, China.
Bi-Sen DingKey Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
Chen WangPeking University China-Japan Friendship School of Clinical Medicine, Beijing, China.
State Key Laboratory of BiotherapyWest China Second University Hospital of Sichuan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular leakage and inflammation are pathological hallmarks of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Endothelial cells (ECs) serve as a semipermeable barrier and play a key role in disease progression. It is well known that fibroblast growth factor receptor 1 (FGFR1) is required for maintaining vascular integrity. However, how endothelial FGFR1 functions in ALI/ARDS remains obscure. Here, we revealed that conditional deletion of endothelial FGFR1 aggravated LPS-induced lung injury, including inflammation and vascular leakage. Inhibition of its downstream Rho-associated coiled-coil-forming protein kinase 2 (ROCK2) by AAV Vec-tie-shROCK2 or its selective inhibitor TDI01 effectively attenuated inflammation and vascular leakage in a mouse model.

Indexed as

Acute Lung InjuryRespiratory Distress SyndromeAnimalsHumansHuman Umbilical Vein Endothelial CellsInflammationLipopolysaccharidesMiceReceptor, Fibroblast Growth Factor, Type 1rho-Associated KinasesUp-RegulationFGFR1 protein, humanLipopolysaccharidesReceptor, Fibroblast Growth Factor, Type 1rho-Associated KinasesROCK2 protein, humanRock2 protein, mouseALI/ARDSendothelial cellFGFR1inflammationROCK2vascular leakage

Identifiers

PMID36969192
PMCPMC10036754
OpenAlexW4323859491

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read66
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 OpenQuestion graph.