Evidence map›Paper›PMID 31853041›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2020

A novel function of calcium sensing receptor in chronic hypoxia-induced pulmonary venous smooth muscle cells proliferation.

Shaoxing Li, Weitao Cao, Wei Hong, Yongliang Jiang, Qiudi Mo, Juan Xu, Rongmin Liu, Wen Tian, Jinxing Hu, Bing Li and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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

12 authors at 8 institutions in 2 countries.

Shaoxing LiGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Weitao CaoGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Wei HongGMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yongliang JiangRespiratory Medicine, Hunan Provincial People's Hospital, Changsha, Hunan, China.
Qiudi MoGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Juan XuGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Rongmin LiuGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Wen TianVA Palo Alto Health Care System, Stanford University School of Medicine, Palo Alto, CA, USA.
Jinxing HuGuangzhou Chest Hospital, Guangzhou, Guangdong, China.
Bing LiGMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Pixin RanGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China. pxran@gzhmu.edu.cn.
Gongyong PengGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China. gongyong19761@163.com.
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNGuangzhou Chest Hospital · CNHunan Provincial People's Hospital · CNPanyu District Central Hospital · CNStanford University · USState Key Laboratory of Respiratory Disease · CNVA Palo Alto Health Care System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hypoxia (CH) causes remodeling not only in pulmonary arteries but also in pulmonary veins. Pulmonary vascular remodeling stems from increased pulmonary vascular myocyte proliferation. However, the pathogenesis of CH-induced proliferation of pulmonary venous smooth muscle cells (PVSMCs) remains unknown. The present study aimed to explore the mechanisms by which CH affects PVSMCs proliferation. PVSMCs were isolated from rat distal pulmonary veins and exposed to CH (4% O

Indexed as

AdamantaneAnimalsCell ProliferationCell SurvivalHypoxiaMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleNaphthalenesPulmonary VeinsQuinoxalinesRatsRats, WistarReceptors, Calcium-SensingUp-RegulationVascular Remodeling2-quinoxaline-carboxamide-N-adamantan-1-ylAdamantaneN-(2-hydroxy-3-(2-cyano-3-chlorophenoxy)propyl)-1,1-dimethyl-2-(2-nephthyl)ethylamineNaphthalenesQuinoxalinesReceptors, Calcium-SensingCalcium sensing receptorHypoxiaProliferationPulmonary veinsPulmonary venous smooth muscle cells

Identifiers

PMID31853041
OpenAlexW2994631704

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.