Evidence map›Paper›PMID 36169661›Full record

ArticleAmerican journal of respiratory cell and molecular biology2022

Neuroblastoma Suppressor of Tumorigenicity 1 Mediates Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension Related to Congenital Heart Disease.

Bin Wen, Rui Peng, Pengxu Kong, Zefu Li, Yao Liu, Wenbin Ouyang, Yongquan Xie, Xiaopeng Hu, Qiang Wang, Xiangbin Pan

Abstract read
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In one paragraph

Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Bin WenDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Rui PengCenter of Clinical Laboratory, Beijing Friendship Hospital, and.
Pengxu KongDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Zefu LiDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Yao LiuDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Wenbin OuyangDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Yongquan XieDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Xiaopeng HuDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Qiang WangDepartment of Pediatric Cardiac Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Xiangbin PanDepartment of Structural Heart Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.ORCID 0000-0002-7090-4414
Chinese Academy of Medical Sciences & Peking Union Medical College · CNBeijing Friendship Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) plays a critical role in the flow-induced vascular remodeling process, such as pulmonary arterial hypertension (PAH) related to congenital heart disease (CHD). NBL1 (neuroblastoma suppressor of tumorigenicity 1) is a secreted glycoprotein that has been implicated in CHD-PAH by aggravating the phenotypic transformation of smooth muscle cells. However, the underlying mechanisms regarding the interplay between NBL1 and endothelial cells in CHD-PAH remain to be fully elucidated. Thus, we aimed to identify the potential effect of NBL1 on EndMT using a novel flow-associated PAH model with

Indexed as

Heart Defects, CongenitalNeuroblastomaPulmonary Arterial HypertensionAnimalsEndothelial CellsEpithelial-Mesenchymal TransitionFamilial Primary Pulmonary HypertensionHumansNerve Tissue ProteinsRatsTransforming Growth Factor betaNbl1 protein, ratNerve Tissue ProteinsTransforming Growth Factor betaEndMTendothelial cellsPAH associated with CHDtransforming growth factor-β/bone morphogenetic protein signaling pathway

Identifiers

PMID36169661
OpenAlexW4297457273

What OpenQuestion 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 OpenQuestion graph.