Evidence map›Paper›PMID 22215517›Full record

ReviewCell stress & chaperones2012

Proteotoxic stress and circulating cell stress proteins in the cardiovascular diseases.

Brian Henderson, A Graham Pockley

Open access · greenAbstract readReview
In one paragraph

Review in Cell stress & chaperones, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Promising Scaffold-Free Approaches in Translational Dentistry.International journal of environmental research and public health · 2020
    Review
  6. Article
  7. Article
  8. Article
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  11. Nox NADPH oxidases and the endoplasmic reticulum.Antioxidants & redox signaling · 2014
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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  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

2 authors at 2 institutions in 1 country.

Brian HendersonDepartment of Microbial Diseases, UCL-Eastman Dental Institute, University College London, London, UK. Brian.Henderson@ucl.ac.uk
A Graham Pockley
Eastman Dental Hospital · GBUniversity of Sheffield · GB

Funding

British Heart Foundation PG/09/014/26950
6 · The paper itself

Abstract

The cardiovasculature is one of the major body systems and probably the one most exposed to stress. There is clear evidence that increasing levels of cell stress proteins within the heart is cardioprotective. In addition, there is rapidly emerging evidence that secreted cell stress proteins play a role in the function of the cardiovascular tissues. Those secreted proteins have three potential functions: (1) as normal homeostatic cardiovascular signals (e.g. protein disulphide isomerase); (2) as anti-inflammatory molecules, which are able to inhibit cardiovascular pathology (e.g. Hsp27); and (iii) as pro-inflammatory signals that can induce and promote cardiovascular pathology (e.g. Hsp60). As all of these various proteins may be released-at different rates-and in different cardiovascular diseases-we need to consider the cohort of potential secreted cell stress proteins as a dynamic system (network) that can aid and/or damage the equally dynamic cardiovascular system.

Indexed as

Autocrine CommunicationCardiovascular DiseasesClusterinHeat-Shock ProteinsHumansParacrine CommunicationThioredoxinsUbiquitinClusterinHeat-Shock ProteinsThioredoxinsUbiquitin

Identifiers

PMID22215517
PMCPMC3312955
OpenAlexW1967077428

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.