Evidence map›Paper›PMID 37337290›Full record

ArticleCell & bioscience2023

A neonatal rat model of pulmonary vein stenosis.

Debao Li, Lisheng Qiu, Haifa Hong, Hao Chen, Peibin Zhao, Yingying Xiao, Hao Zhang, Qi Sun, Lincai Ye

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

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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 2 institutions in 1 country.

Debao Li *Department of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University, 1678 Dongfang Road, Shanghai, 200127, China.
Lisheng Qiu *Department of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University, 1678 Dongfang Road, Shanghai, 200127, China.
Haifa Hong *Department of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Hao ChenDepartment of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University, 1678 Dongfang Road, Shanghai, 200127, China.
Peibin ZhaoInstitute of Cardiovascular Development and Translational Medicine, Children's Heart Center, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Yingying XiaoDepartment of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Hao ZhangInstitute of Cardiovascular Development and Translational Medicine, Children's Heart Center, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, China. drzhanghao@163.com.
Qi SunDepartment of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University, 1678 Dongfang Road, Shanghai, 200127, China. empyrealheights@163.com.
Lincai YeDepartment of Thoracic and Cardiovascular Surgery, School of Medicine, Shanghai Children's Medical Center, Shanghai Jiao Tong University, 1678 Dongfang Road, Shanghai, 200127, China. ylc717@163.com.ORCID http://orcid.org/0000-0001-8808-2810
Shanghai Jiao Tong University · CNWenzhou Medical University · CN

Funding

Foundation of Pudong Science and Technology Development PKJ2019-Y12Health and Family Planning Committee of Pudong New Area PWZxq2017-14Innovation Project of Distinguished Medical Team in Ningbo 2022020405National Key R&D Program of China 2019YFA0110401National Natural Science Foundation of China 82001835National Natural Science Foundation of China 82200309National Natural Science Foundation of China 82270314Natural Science Foundation of Shanghai 22ZR147900Natural Science Foundation of Shanghai 23ZR1441100Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 19411950200Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 201409005900Shanghai Key Clinical Specialty(shslczdzk), Biomedical and Engineering (Science) Interdisciplinary Study Fund of Shanghai Jiaotong University YG2019QNB03
6 · The paper itself

Abstract

objectivesPulmonary vein stenosis (PVS), one of the most challenging clinical problems in congenital heart disease, leads to secondary pulmonary arterial hypertension (PAH) and right ventricular (RV) hypertrophy. Due to the lack of a rodent model, the mechanisms underlying PVS and its associated secondary effects are largely unknown, and treatments are minimally successful. This study developed a neonatal rat PVS model with the aim of increasing our understanding of the mechanisms and developing possible treatments for PVS.

methodsPVS was created at postnatal day 1 (P1) by banding pulmonary veins that receive blood from the right anterior and mid lobes. The condition was confirmed using echocardiography, computed tomography (CT), gross anatomic examination, hematoxylin and eosin (H&E) staining, fibrosis staining, and immunofluorescence. Lung and RV remodeling under the condition of PVS were evaluated using H&E staining, fibrosis staining, and immunofluorescence.

resultsAt P21, echocardiography revealed a change in wave form and a decrease in pulmonary artery acceleration time-indicators of PAH-at the transpulmonary valve site in the PVS group. CT at P21 showed a decrease in pulmonary vein diameter in the PVS group. At P30 in the PVS group, gross anatomic examination showed pulmonary congestion, H&E staining showed wall thickening and lumen narrowing in the upstream pulmonary veins, and immunofluorescence showed an increase in the smooth muscle layers in the upstream pulmonary veins. In addition, at P30 in the PVS group, lung remodeling was evidenced by hyperemia, thickening of pulmonary small vessel walls and smooth muscle layers, and reduction of the number of alveoli. RV remodeling was evidenced by an increase in RV free wall thickness.

conclusionsA neonatal rat model of PVS was successfully established, showing secondary lung and RV remodeling. This model may serve as a useful platform for understanding the mechanisms and treatments for PVS.

Indexed as

Congenital heart diseaseIntimal hyperplasiaLung remodelingPulmonary arterial hypertensionPulmonary vein stenosisRight ventricular hypertrophy

Identifiers

PMID37337290
PMCPMC10278335
OpenAlexW4381250230

What OpenQuestion holds

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LicenceCC BY
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.