Evidence map›Paper›PMID 32357544›Full record

ReviewCells2020

Biomaterials to Neuroprotect the Stroke Brain: A Large Opportunity for Narrow Time Windows.

Daniel González-Nieto, Rocío Fernández-Serra, José Pérez-Rigueiro, Fivos Panetsos, Ricardo Martinez-Murillo, Gustavo V Guinea

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  9. Non-human primate models of focal cortical ischemia for neuronal replacement therapy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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  15. Pharmacological Effect ofBioMed research international · 2022
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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

6 authors at 4 institutions in 1 country.

Daniel González-NietoCenter for Biomedical Technology, Universidad Politécnica de Madrid, 28040 Madrid, Spain.
Rocío Fernández-SerraCenter for Biomedical Technology, Universidad Politécnica de Madrid, 28040 Madrid, Spain.ORCID 0000-0002-7362-117X
José Pérez-RigueiroCenter for Biomedical Technology, Universidad Politécnica de Madrid, 28040 Madrid, Spain.
Fivos PanetsosNeurocomputing and Neurorobotics Research Group: Faculty of Biology and Faculty of Optics, Universidad Complutense de Madrid, 28040 Madrid, Spain.ORCID 0000-0003-0897-411X
Ricardo Martinez-MurilloDepartment of Translational Neuroscience, Instituto Cajal (CSIC), 28002 Madrid, Spain.
Gustavo V GuineaCenter for Biomedical Technology, Universidad Politécnica de Madrid, 28040 Madrid, Spain.
Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESInstituto Cajal · ESUniversidad Complutense de Madrid · ESUniversidad Politécnica de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke represents one of the most prevalent pathologies in humans and is a leading cause of death and disability. Anti-thrombolytic therapy with tissue plasminogen activator (t-PA) and surgical thrombectomy are the primary treatments to recanalize occluded vessels and normalize the blood flow in ischemic and peri-ischemic regions. A large majority of stroke patients are refractory to treatment or are not eligible due to the narrow time window of therapeutic efficacy. In recent decades, we have significantly increased our knowledge of the molecular and cellular mechanisms that inexorably lead to progressive damage in infarcted and peri-lesional brain areas. As a result, promising neuroprotective targets have been identified and exploited in several stroke models. However, these considerable advances have been unsuccessful in clinical contexts. This lack of clinical translatability and the emerging use of biomaterials in different biomedical disciplines have contributed to developing a new class of biomaterial-based systems for the better control of drug delivery in cerebral disorders. These systems are based on specific polymer formulations structured in nanoparticles and hydrogels that can be administered through different routes and, in general, bring the concentrations of drugs to therapeutic levels for prolonged times. In this review, we first provide the general context of the molecular and cellular mechanisms impaired by cerebral ischemia, highlighting the role of excitotoxicity, inflammation, oxidative stress, and depolarization waves as the main pathways and targets to promote neuroprotection avoiding neuronal dysfunction. In the second part, we discuss the versatile role played by distinct biomaterials and formats to support the sustained administration of particular compounds to neuroprotect the cerebral tissue at risk of damage.

Indexed as

Biocompatible MaterialsBrainBrain IschemiaDrug Delivery SystemsHumansInflammationNanoparticlesNeuroprotectionNeuroprotective AgentsOxidative StressStrokeThrombolytic TherapyTissue Plasminogen ActivatorBiocompatible MaterialsNeuroprotective AgentsTissue Plasminogen Activatorbiomaterialsbrain ischemiadrug deliveryexcitotoxicityhydrogelsinflammationnanoparticlesneuroprotectionoxidative stresspolymersspreading depressionstroke

Identifiers

PMID32357544
PMCPMC7291200
OpenAlexW3019391302

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.