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.
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.
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.
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.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- The pivotal role of β-lactone stereochemistry in the development of SARS-CoV-2 MProtein science : a publication of the Protein Society · 2026Article
- The Transcription Axes ERK-Elk1, JNK-cJun, and JAK-STAT Promote Autophagy Activation and Proteasome Inhibitor Resistance in Prostate Cancer Cells.Current issues in molecular biology · 2025Article
- Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury.Molecular biology reports · 2024Review
- Improvement of postoperative cognitive dysfunction and attention network function of patients with ischemic cerebrovascular disease via dexmedetomidine.Experimental and therapeutic medicine · 2018Article
- Systemic Proteasome Inhibition Induces Sustained Post-stroke Neurological Recovery and Neuroprotection via Mechanisms Involving Reversal of Peripheral Immunosuppression and Preservation of Blood-Brain-Barrier Integrity.Molecular neurobiology · 2016Article
- Inhibition of Proteasome Activity Induces Formation of Alternative Proteasome Complexes.The Journal of biological chemistry · 2016Article
- CHIP Is an Essential Determinant of Neuronal Mitochondrial Stress Signaling.Antioxidants & redox signaling · 2015Article
- Role of the proteasome in excitotoxicity-induced cleavage of glutamic acid decarboxylase in cultured hippocampal neurons.PloS one · 2010Article
- Article
- Proteasome inhibitors prevent oxidative stress-induced nerve cell death by a novel mechanism.Biochemical pharmacology · 2008Article
- 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 · 2007Review
- Proteasome inhibitors: antitumor effects and beyond.Leukemia · 2007Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
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
Identifiers
16044664PMC2880390W2285195207What OpenQuestion holds
Registered trials
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.