Evidence map›Paper›PMID 20840877›Full record

ReviewBiochimica et biophysica acta2011

The role of the proteasome in heart disease.

Yi-Fan Li, Xuejun Wang

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Proteasome biology and therapeutics in cardiac diseases.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  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 1 institution in 1 country.

Yi-Fan LiDivision of Basic, Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD 57069, USA.
Xuejun Wang
University of South Dakota · US

Funding

Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
PROTEIN OXIDATION AND CARDIAC CONTRACTILE DYSFUNCTIONR01HL068936 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI POWELL, SAUL R, WANG, XUEJUN · 2003 to 2011
$3.2M
Vagus stimulation protects against cardiac diastolic dysfunction in aging miceR03AG033291 · NIA · UNIVERSITY OF SOUTH DAKOTA · PI LI, YIFAN · 2009 to 2010
$118k
NHLBI NIH HHS R01 HL068936NHLBI NIH HHS R01HL068936NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01HL085629NIA NIH HHS R03 AG033291NIA NIH HHS R03AG033291
6 · The paper itself

Abstract

Intensive investigations into the pathophysiological significance of the proteasome in the heart did not start until the beginning of the past decade but exciting progress has been made and summarized here as two fronts. First, strong evidence continues to emerge to support a novel hypothesis that proteasome functional insufficiency represents a common pathological phenomenon in a large subset of heart disease, compromises protein quality control in heart muscle cells, and thereby acts as a major pathogenic factor promoting the progression of the subset of heart disease to congestive heart failure. This front is represented by the studies on the ubiquitin-proteasome system (UPS) in cardiac proteinopathy, which have taken advantage of a transgenic mouse model expressing a fluorescence reporter for UPS proteolytic function. Second, pharmacological inhibition of the proteasome has been explored experimentally as a potential therapeutic strategy to intervene on some forms of heart disease, such as pressure-overload cardiac hypertrophy, viral myocarditis, and myocardial ischemic injury. Not only between the two fronts but also within each one, a multitude of inconsistencies and controversies remain to be explained and clarified. At present, the controversy perhaps reflects the sophistication of cardiac proteasomes in terms of the composition, assembly, and regulation, as well as the intricacy and diversity of heart disease in terms of its etiology and pathogenesis. A definitive role of altered proteasome function in the development of various forms of heart disease remains to be established. This article is part of a Special Issue entitled The 26S Proteasome: When degradation is just not enough!

Indexed as

AnimalsDoxorubicinHeart DiseasesHumansMyocardial IschemiaMyocardiumProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalDoxorubicinProteasome Endopeptidase Complex

Identifiers

PMID20840877
PMCPMC3021001
OpenAlexW1968975143

What OpenQuestion holds

Textmetadata
LicenceTDM
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.