Evidence map›Paper›PMID 17681036›Full record

ReviewAging cell2007

Aging and regulated protein degradation: who has the UPPer hand?

Vita A Vernace, Thomas Schmidt-Glenewinkel, Maria E Figueiredo-Pereira

Abstract readReview
In one paragraph

Review in Aging cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. International journal of molecular sciences · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. The Critical Role of Oxidative Stress in Sarcopenic Obesity.Oxidative medicine and cellular longevity · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Pharmacology of manipulating lean body mass.Clinical and experimental pharmacology & physiology · 2015
    Review
  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.

Vita A VernaceDepartment of Biological Sciences, Hunter College of the City University of New York, New York, NY 10021, USA.
Thomas Schmidt-Glenewinkel
Maria E Figueiredo-Pereira

Funding

WILD TYPE &MUTANT P53 INTERACTIONS WITH HIV LTR DNAG12RR003037 · NCRR · HUNTER COLLEGE · PI DOTTIN, ROBERT P · 1985 to 2011
$27.6M
UBIQUITINATED PROTEIN DEGRADATION AND NEURODEGENERATIONS06GM060654 · NIGMS · HUNTER COLLEGE · PI LUINE, VICTORIA N · 2000 to 2011
$21.2M
SNRP AT HUNTER COLLEGEU54NS041073 · NINDS · HUNTER COLLEGE · PI FILBIN, MARIE T. · 2000 to 2010
$16.4M
NCRR NIH HHS G12 RR003037NCRR NIH HHS RR03037NIGMS NIH HHS GM60654NIGMS NIH HHS S06 GM060654NINDS NIH HHS NS41073NINDS NIH HHS U54 NS041073
6 · The paper itself

Abstract

In all cells, protein degradation is a constant, ongoing process that is critical for cell survival and repair. The ubiquitin/proteasome pathway (UPP) is the major proteolytic pathway that degrades intracellular proteins in a regulated manner. It plays critical roles in many cellular processes and diseases. Disruption of the UPP is particularly relevant to pathophysiological conditions that provoke the accumulation of aberrant proteins, such as in aging as well as in a variety of neurodegenerative disorders including Alzheimer's and Parkinson's diseases. For unknown reasons, most of these neurodegenerative disorders that include familial and sporadic cases exhibit a late onset. It is possible that these neurodegenerative conditions exhibit a late onset because proteasome activity decreases with aging. Aging-dependent impairment in proteolysis mediated by the proteasome may have profound ramifications for cell viability. It can lead to the accumulation of modified, potentially toxic proteins in cells and can cause cell injury or premature cell death by apoptosis or necrosis. While it is accepted that aging affects UPP function, the question is why does aging cause a decline in regulated protein degradation by the UPP? Herein, we review some of the properties of the UPP and mechanisms mediating its age-dependent impairment. We also discuss the relevance of these findings leading to a model that proposes that UPP dysfunction may be one of the milestones of aging.

Indexed as

AgingAnimalsHumansProteasome Endopeptidase ComplexProteinsUbiquitinProteasome Endopeptidase ComplexProteinsUbiquitin

Identifiers

PMID17681036
PMCPMC3464091

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.