Evidence map›Paper›PMID 40391857›Full record

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

Mechanical Stress Induced NOX2 Promotes Endothelial Dysfunction in Ventilator-Induced Lung Injury: Potential Treatment with Quercetin.

Tao Jiang, Yabing Zhang, Zhiye Guo, He Ren, Weiyi Hu, Qingping Yao, Yunlong Huo, Yingxin Qi, Kai Huang

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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.

Tao JiangInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Yabing ZhangDepartment of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Zhiye GuoInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
He RenInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Weiyi HuInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Qingping YaoInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Yunlong HuoInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Yingxin QiInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.
Kai HuangInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, Shanghai, 200240, China.ORCID https://orcid.org/0009-0001-2257-0843

Funding

National Key Research and Development Program of China 2021YFA1000200National Key Research and Development Program of China 2021YFA1000203National Natural Science Foundation of China 12032003National Natural Science Foundation of China 12302409National Natural Science Foundation of China 12372313
6 · The paper itself

Abstract

Mechanical ventilation (MV) is a treatment that helps people who are unable to breathe on their own. However, the use of MV leads to the development of ventilator-induced lung injury (VILI). Here, it is found that VILI with endothelial barrier disruption is accompanied by elevated reactive oxygen species (ROS) in mice. NADPH oxidase 2 (NOX2, also known as CYBB or gp91phox) is first examined to be the main source of ROS to repress endothelial junction. Besides, 20%-0.5 Hz high cyclic stretch (high CS) significantly increases NOX2 expression and inhibits endothelial junction protein expression. NOX2 activates the downstream Calcium-calmodulin (CaM)-dependent protein kinase II (CaMKII)/ Extracellular signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway through the regulation of ROS. This pathway is confirmed by high MV stimulation in vivo and high CS in vitro. Of note, quercetin, as an antioxidant, is effective in preventing mechanical stretch-induced endothelial dysfunction by scavenging ROS. Omics data indicated that there is a similar gene expression pattern in cecal ligation and puncture (CLP) and VILI. Pre-administration of quercetin significantly improves the survival rate of mice via inactivating ROS/CaMKII/ERK1/2 axis. Quercetin pre-treatment not only preventes MV-induced lung injury but also attenuates existing inflammation-induced lung injury.

Indexed as

NADPH Oxidase 2QuercetinStress, MechanicalVentilator-Induced Lung InjuryAnimalsAntioxidantsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLReactive Oxygen SpeciesAntioxidantsCybb protein, mouseNADPH Oxidase 2QuercetinReactive Oxygen Speciesendothelial barrier dysfunctionendothelial cells (ECs)mechanical stressmechanotransductionNADPH oxidase (NOX)quercetinreactive oxygen species (ROS)ventilator‐induced lung injury (VILI)

Identifiers

PMID40391857
PMCPMC12302586

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Registered trials

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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.