Evidence map›Paper›PMID 32509157›Full record

ReviewAmerican journal of translational research2020

A crucial role of endoplasmic reticulum stress in cellular responses during pulmonary arterial hypertension.

Ting Pan, Lei Zhang, Kang Miao, Yi Wang

Open access · greenAbstract readReview
In one paragraph

Review in American journal of translational research, 2020. 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
1.1field-weighted citation impact, top 19% 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, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Oxidative Stress and Hypertension.Circulation research · 2021
    Review
  11. 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

4 authors at 1 institution in 1 country.

Ting PanDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology 1095 Jiefang Ave, Wuhan 430030, China.
Lei ZhangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology 1095 Jiefang Ave, Wuhan 430030, China.
Kang MiaoDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology 1095 Jiefang Ave, Wuhan 430030, China.
Yi WangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Cite of National Clinical Research Center for Respiratory Disease, Wuhan Clinical Medical Research Center for Chronic Airway Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology 1095 Jiefang Ave, Wuhan 430030, China.
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH), a chronic and progressive disease of the lung vascular system, is characterized by vasculopathy in the pulmonary arterioles, especially in endothelial cells and pulmonary vascular smooth cells. Several mechanisms are involved in PAH occurrence and development, and all are characterized by excessive pulmonary vasoconstriction and abnormal vascular remodeling, which leads to a progressive resistance to blood flow and an increase in pulmonary artery pressure. Recent studies have shown that endoplasmic reticulum (ER) stress is implicated in the pathophysiology of PAH. In this review, we highlight the effect of ER stress on the proliferation and apoptosis of endothelial cells and pulmonary vascular smooth muscle cells, and discuss the feasibility of targeting unfolded protein response components as a strategy to reverse or alleviate the progression of PAH.

Indexed as

endoplasmic reticulum (ER) stressendothelial cells (ECs)Pulmonary arterial hypertension (PAH)pulmonary artery smooth muscle cells (PASMCs)unfolded protein response (UPR)

Identifiers

PMID32509157
PMCPMC7269988
OpenAlexW3033871832

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.