Evidence map›Paper›PMID 20411034›Full record

ArticleInternational journal of physiology, pathophysiology and pharmacology2009

Interplay between the ubiquitin-proteasome system and autophagy in proteinopathies.

Qingwen Zheng, Jie Li, Xuejun Wang

Abstract read
In one paragraph

Article in International journal of physiology, pathophysiology and pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023
    Article
  5. Review
  6. An Update on Autophagy in Prion Diseases.Frontiers in bioengineering and biotechnology · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The fine-tuning of proteolytic pathways in Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. α -Synuclein Modification in an ALS Animal Model.Evidence-based complementary and alternative medicine : eCAM · 2013
    Article
  19. 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

3 authors at 1 institution in 1 country.

Qingwen ZhengDivision of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota 414 East Clark Street, Vermillion, SD 57069, USA.
Jie Li
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
NHLBI NIH HHS R01 HL068936NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL085629
6 · The paper itself

Abstract

Proteinopathies are a family of human disease caused by toxic aggregation-prone proteins and featured by the presence of protein aggregates in the affected cells. The ubiquitin-proteasome system (UPS) and autophagy are two major intracellular protein degradation pathways. The UPS mediates the targeted degradation of most normal proteins after performing their normal functions as well as the removal of abnormal, soluble proteins. Autophagy is mainly responsible for degradation of defective organelles and the bulk degradation of cytoplasm during starvation. The collaboration between the UPS and autophagy appears to be essential to protein quality control in the cell. UPS proteolytic function often becomes inadequate in proteinopathies which may lead to activation of autophagy, striving to remove abnormal proteins especially the aggregated forms. HADC6, p62, and FoxO3 may play an important role in mobilizing this proteolytic consortium. Benign measures to enhance proteasome function are currently lacking; however, enhancement of autophagy via pharmacological intervention and/or lifestyle change has shown great promise in alleviating bona fide proteinopathies in the cell and animal models. These pharmacological interventions are expected to be applied clinically to treat human proteinopathies in the near future.

Indexed as

autophagyFoxO3HADC6p62proteinopathyUbiquitin proteasome system

Identifiers

PMID20411034
PMCPMC2856956
OpenAlexW166887533

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.