Evidence map›Paper›PMID 22727426›Full record

ReviewProgress in molecular biology and translational science2012

The ubiquitin-proteasome system and cardiovascular disease.

Saul R Powell, Joerg Herrmann, Amir Lerman, Cam Patterson, Xuejun Wang

Open access · greenAbstract readReview
In one paragraph

Review in Progress in molecular biology and translational science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
15.6field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Proteostasis signatures in human diseases.PLoS computational biology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Ubiquitin Proteasome System Role in Diabetes-Induced Cardiomyopathy.International journal of molecular sciences · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Article
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  20. Review
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

5 authors at 4 institutions in 1 country.

Saul R PowellCenter for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA.
Joerg Herrmann
Amir Lerman
Cam Patterson
Xuejun Wang
Mayo Clinic · USFeinstein Institute for Medical Research · USUniversity of North Carolina at Chapel Hill · USUniversity 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
Myocyte Signaling and the Response to StressR37HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2010 to 2019
$3.7M
CHIP: A link between the chaperone &proteasome systemsR01GM061728 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SCHISLER, JONATHAN C. · 2001 to 2013
$3.4M
PROTEIN OXIDATION AND CARDIAC CONTRACTILE DYSFUNCTIONR01HL068936 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI POWELL, SAUL R, WANG, XUEJUN · 2003 to 2011
$3.2M
Myocyte signaling and the response to stressR01HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2001 to 2009
$2.7M
Lp-PLA2 and Coronary Atherosclerosis in HumansR01HL092954 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, AMIR · 2009 to 2013
$2.1M
Role of Endothelial Progenitor Cells in vascular Aging and CalcificationR01AG031750 · NIA · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP, LERMAN, AMIR · 2010 to 2014
$2.0M
NHLBI NIH HHS HL065619NHLBI NIH HHS HL 68936NHLBI NIH HHS HL72166NHLBI NIH HHS HL85629NHLBI NIH HHS HL 92954NHLBI NIH HHS R01 HL065619NHLBI NIH HHS R01 HL068936NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01 HL092954NHLBI NIH HHS R37 HL065619NIA NIH HHS AG 31750NIA NIH HHS R01 AG031750NIGMS NIH HHS GM061728NIGMS NIH HHS R01 GM061728
6 · The paper itself

Abstract

Over the past decade, the role of the ubiquitin-proteasome system (UPS) has been the subject of numerous studies to elucidate its role in cardiovascular physiology and pathophysiology. There have been many advances in this field including the use of proteomics to achieve a better understanding of how the cardiac proteasome is regulated. Moreover, improved methods for the assessment of UPS function and the development of genetic models to study the role of the UPS have led to the realization that often the function of this system deviates from the norm in many cardiovascular pathologies. Hence, dysfunction has been described in atherosclerosis, familial cardiac proteinopathies, idiopathic dilated cardiomyopathies, and myocardial ischemia. This has led to numerous studies of the ubiquitin protein (E3) ligases and their roles in cardiac physiology and pathophysiology. This has also led to the controversial proposition of treating atherosclerosis, cardiac hypertrophy, and myocardial ischemia with proteasome inhibitors. Furthering our knowledge of this system may help in the development of new UPS-based therapeutic modalities for mitigation of cardiovascular disease.

Indexed as

Cardiovascular DiseasesHumansModels, CardiovascularMyocardiumProteasome Endopeptidase ComplexProteasome InhibitorsUbiquitinUbiquitin-Protein LigasesProteasome Endopeptidase ComplexProteasome InhibitorsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID22727426
PMCPMC3743449
OpenAlexW52775975

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.