Evidence map›Paper›PMID 20167943›Full record

ReviewCirculation research2010

Sent to destroy: the ubiquitin proteasome system regulates cell signaling and protein quality control in cardiovascular development and disease.

Monte S Willis, W H Davin Townley-Tilson, Eunice Y Kang, Jonathon W Homeister, Cam Patterson

Abstract readReview
In one paragraph

Review in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
14.2field-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

118 citing papers in PubMed, 206 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. CYLD in health and disease.Disease models & mechanisms · 2023
    Review
  18. Review
  19. Cardiac-specific ITCH overexpression ameliorates septic cardiomyopathyJournal of molecular and cellular cardiology plus · 2022
    Article
  20. Article

58 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Monte S WillisDivision of Cardiology, McAllister Heart Institute, University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599-7126, USA.
W H Davin Townley-Tilson
Eunice Y Kang
Jonathon W Homeister
Cam Patterson
Cardiovascular Institute of the South · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
Pre-doctoral Training Program in Integrative Vascular BiologyT32HL069768 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Christopher P. Mack · 2002 to 2026
$9.7M
Signaling in endothelial growth & angiogenesisR01HL061656 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PI, XINCHUN · 1999 to 2017
$5.8M
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
Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
Myocyte signaling and the response to stressR01HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2001 to 2009
$2.7M
UNC-Clinician-Scientist Training Program in Cardiovascular MedicineT32HL083828 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STOUFFER, GEORGE A · 2006 to 2015
$2.0M
Selectin-dependent lineage-specific leukocyte recruitment in atherogenesis.R01HL090823 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HOMEISTER, JONATHON · 2008 to 2012
$1.6M
NHLBI NIH HHS R01 HL061656NHLBI NIH HHS R01HL061656NHLBI NIH HHS R01 HL065619NHLBI NIH HHS R01HL065619NHLBI NIH HHS R01 HL090823NHLBI NIH HHS R01 HL104129NHLBI NIH HHS R37 HL065619NHLBI NIH HHS T32 HL069768NHLBI NIH HHS T32 HL083828NIEHS NIH HHS P30 ES010126NIGMS NIH HHS R01 GM061728NIGMS NIH HHS R01GM061728
6 · The paper itself

Abstract

The ubiquitin proteasome system (UPS) plays a crucial role in biological processes integral to the development of the cardiovascular system and cardiovascular diseases. The UPS prototypically recognizes specific protein substrates and places polyubiquitin chains on them for subsequent destruction by the proteasome. This system is in place to degrade not only misfolded and damaged proteins, but is essential also in regulating a host of cell signaling pathways involved in proliferation, adaptation to stress, regulation of cell size, and cell death. During the development of the cardiovascular system, the UPS regulates cell signaling by modifying transcription factors, receptors, and structural proteins. Later, in the event of cardiovascular diseases as diverse as atherosclerosis, cardiac hypertrophy, and ischemia/reperfusion injury, ubiquitin ligases and the proteasome are implicated in protecting and exacerbating clinical outcomes. However, when misfolded and damaged proteins are ubiquitinated by the UPS, their destruction by the proteasome is not always possible because of their aggregated confirmations. Recent studies have discovered how these ubiquitinated misfolded proteins can be destroyed by alternative "specific" mechanisms. The cytosolic receptors p62, NBR, and histone deacetylase 6 recognize aggregated ubiquitinated proteins and target them for autophagy in the process of "selective autophagy." Even the ubiquitination of multiple proteins within whole organelles that drive the more general macro-autophagy may be due, in part, to similar ubiquitin-driven mechanisms. In summary, the crosstalk between the UPS and autophagy highlight the pivotal and diverse roles the UPS plays in maintaining protein quality control and regulating cardiovascular development and disease.

Indexed as

AnimalsApoptosisAtherosclerosisBlood VesselsCardiovascular DiseasesCholesterolHumansLysosomesMiceMuscle ProteinsMyocardiumNeoplasm ProteinsOxidative StressProteasome Endopeptidase ComplexRatsReceptors, NotchCholesterolMuscle ProteinsNeoplasm ProteinsProteasome Endopeptidase ComplexReceptors, NotchrecogninsUbiquitin

Identifiers

PMID20167943
PMCPMC2826711
OpenAlexW2052735334

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.