Evidence map›Paper›PMID 33934111›Full record

ArticleCell death & disease2021

Intermedin

Jin-Ling Ren, Yao Chen, Lin-Shuang Zhang, Ya-Rong Zhang, Shi-Meng Liu, Yan-Rong Yu, Mo-Zhi Jia, Chao-Shu Tang, Yong-Fen Qi, Wei-Wei Lu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. IntermedinJournal of inflammation research · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Endogenous Vasoactive Peptides and Vascular Aging-Related Diseases.Oxidative medicine and cellular longevity · 2022
    Review
  18. Review
  19. Review
  20. 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

10 authors at 3 institutions in 2 countries.

Jin-Ling RenKey Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University Health Science Center, 100191, Beijing, China.
Yao ChenDepartment of Physiology, School of Basic Medical Sciences, Chongqing Medical University, 400016, Chongqing, China.
Lin-Shuang ZhangDepartment of Pathogen Biology, School of Basic Medical Sciences, Peking University Health Science Center, 100191, Beijing, China.
Ya-Rong ZhangDepartment of Pathogen Biology, School of Basic Medical Sciences, Peking University Health Science Center, 100191, Beijing, China.
Shi-Meng LiuDepartment of Pathogen Biology, School of Basic Medical Sciences, Peking University Health Science Center, 100191, Beijing, China.
Yan-Rong YuDepartment of Pathogen Biology, School of Basic Medical Sciences, Peking University Health Science Center, 100191, Beijing, China.
Mo-Zhi JiaDepartment of Pathogen Biology, School of Basic Medical Sciences, Peking University Health Science Center, 100191, Beijing, China.
Chao-Shu TangKey Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University Health Science Center, 100191, Beijing, China.
Yong-Fen QiKey Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University Health Science Center, 100191, Beijing, China. yongfenqi@163.com.ORCID 0000-0001-6514-0491
Wei-Wei LuDepartment of Physiology and Neurobiology, Medical College of Soochow University, 215123, Suzhou, China. wwlu@suda.edu.cn.ORCID 0000-0002-1982-390X
Peking University · CNChongqing Medical University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerotic plaque vulnerability and rupture increase the risk of acute coronary syndromes. Advanced lesion macrophage apoptosis plays important role in the rupture of atherosclerotic plaque, and endoplasmic reticulum stress (ERS) has been proved to be a key mechanism of macrophage apoptosis. Intermedin (IMD) is a regulator of ERS. Here, we investigated whether IMD enhances atherosclerotic plaque stability by inhibiting ERS-CHOP-mediated apoptosis and subsequent inflammasome in macrophages. We studied the effects of IMD on features of plaque vulnerability in hyperlipemia apolipoprotein E-deficient (ApoE

Indexed as

AnimalsApoptosisHumansInflammasomesMacrophagesMiceNeuropeptidesPeptide FragmentsPlaque, AtheroscleroticInflammasomesintermedin protein, mouseNeuropeptidesPeptide Fragments

Identifiers

PMID33934111
PMCPMC8088440
OpenAlexW3159614175

What OpenQuestion holds

Textmetadata
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.