ReviewMolecular neurobiology2003
Molecular pathways in cerebral ischemia: cues to novel therapeutic strategies.
Review in Molecular neurobiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
11 citing papers in PubMed.
- The Association between Hypoxia-Induced Low Activity and Apoptosis Strongly Resembles That between TTX-Induced Silencing and Apoptosis.International journal of molecular sciences · 2022Article
- Therapeutic Potential of Pretreatment with Allograft Sertoli Cells Transplantation in Brain Ischemia by Improving Oxidative Defenses.Journal of molecular neuroscience : MN · 2018Article
- Imidazol-1-ylethylindazole voltage-gated sodium channel ligands are neuroprotective during optic neuritis in a mouse model of multiple sclerosis.Journal of medicinal chemistry · 2014Article
- All's well that transcribes well: non-coding RNAs and post-stroke brain damage.Neurochemistry international · 2013Review
- Therapeutic targets for neuroprotection in acute ischemic stroke: lost in translation?Antioxidants & redox signaling · 2011Review
- Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia.Acta pharmacologica Sinica · 2011Article
- Prediction of the survival and functional ability of severe stroke patients after ICU therapeutic intervention.BMC neurology · 2008Article
- Blood biologic markers of stroke: improved management, reduced cost?Current atherosclerosis reports · 2006Review
- Altered responsiveness of the guinea-pig isolated ileum to smooth muscle stimulants and to electrical stimulation after in situ ischemia.British journal of pharmacology · 2006Article
- A novel adenoviral vector which mediates hypoxia-inducible gene expression selectively in neurons.Gene therapy · 2005Article
- The design of clinical trials for cell transplantation into the central nervous system.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is one of the leading causes of death and severe disability in most industrialized countries. Despite the extensive research efforts of both academic and industrial laboratories during the last few decades, no changes have been brought about by the design of neuroprotective therapies. The progressive decrease of stroke-induced death and disability is entirely attributable to improvements in the identification and reduction of risk factors. Over the past few years, experimental research has led to the emergence of a wealth of information regarding the complex and interrelated processes of neuronal degeneration and death triggered by ischemia. This unprecedented insight has led to new theories on the mechanisms of ischemic damage, and has suggested new targets and strategies for therapeutic intervention designed to reduce the clinical consequences of stroke. Among current developments, three strategies seem particularly appealing namely, the limitation of initial or secondary neuronal death by inhibition of apoptotic mechanisms, the enhancement of the endogenous capacity of nervous structures to restore lost function, and the replacement of lost cells by transplantation therapy.
Indexed as
Identifiers
12668901What 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.