Evidence map›Paper›PMID 16044664›Full record

ReviewCurrent opinion in investigational drugs (London, England : 2000)2005

The ubiquitin-proteasome system as a drug target in cerebrovascular disease: therapeutic potential of proteasome inhibitors.

Mario Di Napoli, BethAnn McLaughlin

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Current opinion in investigational drugs (London, England : 2000), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. The pivotal role of β-lactone stereochemistry in the development of SARS-CoV-2 MProtein science : a publication of the Protein Society · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Killer proteases and little strokes--how the things that do not kill you make you stronger.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2007
    Review
  13. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

2 authors.

Mario Di NapoliNeurological Section, SMDN-Center for Cardiovascular Medicine and Cerebrovascular Disease Prevention, Via Trento, 41 67039 Sulmona (AQ), Italy. mariodinapoli@katamail.com
BethAnn McLaughlin

Funding

THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI DYKENS, ELISABETH MAY · 1985 to 2014
$18.6M
BIOCHEMISTRY AND PHARMACOLOGY OF D2/E2-ISOPROSTANESR01DK048831 · NIDDK · VANDERBILT UNIVERSITY · PI YIN, HUIYONG · 1995 to 2008
$2.2M
Cellular Mechanisms of Preconditioning NeuroprotectionR01NS050396 · NINDS · VANDERBILT UNIVERSITY · PI MCLAUGHLIN, BETHANN M · 2005 to 2009
$1.7M
NICHD NIH HHS P30 HD015052NICHD NIH HHS P30HD15052NIDDK NIH HHS R01 DK048831NINDS NIH HHS R01 NS050396
6 · The paper itself

Abstract

Proteasomes are large, multi-catalytic protease complexes that are found in the cytosol and in the nucleus of eukaryotic cells with a central role in cellular protein turnover. The ubiquitin-proteasome system (UPS) is the predominant non-lysosomal protein degradation pathway that ensures the viability, proliferation and signaling of eukaryotic organisms. Overwhelming data exist implicating a critical role for the UPS in cerebral ischemic injury. Ischemic and hypoxic trauma, and their associated oxidative, nitrosylative and energetic stress, underlie neurodegeneration following stroke, and evoke a discreet set of transcriptional events which have a complex and interdependent relationship with proteasomal function. Rapid elimination of denatured, misfolded and damaged proteins by the proteasome becomes a critical determinant of cell fate. Proof-of-principle has been obtained from animal models of cerebral ischemia, in which proteasome inhibitors reduce neuronal and astrocytic degeneration, cortical infarct volume, infarct neutrophil infiltration. and nuclear factor kappaB immunoreactivity. This neuroprotective efficacy has also been observed when proteasome inhibitors have been used 6 h after ischemic insult. Strategies aimed at effecting long-lasting changes in proteasomal function are not recommended, given the growing body of evidence implicating long-term proteasomal dysfunction in chronic neurodegenerative disease. These effects are likely due to the fact that the UPS is also essential for cellular growth, metabolism and repair, and untoward effects of proteasomal inhibition indicate that the development of short-lived proteasome inhibitors, or compounds which can spatially and temporally regulate the UPS, is a desirable clinical target. Studies in animal models indicate that the use of specific proteasome inhibitors may be beneficial in treating a host of acute neurological disorders, including ischemic stroke.

Indexed as

Proteasome InhibitorsAnimalsCerebrovascular DisordersDisease Models, AnimalHumansProtease InhibitorsProteasome Endopeptidase ComplexUbiquitinProtease InhibitorsProteasome Endopeptidase ComplexProteasome InhibitorsUbiquitin

Identifiers

PMID16044664
PMCPMC2880390
OpenAlexW2285195207

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.