Evidence map›Paper›PMID 29318974›Full record

ReviewCurrent neuropharmacology2018

Understanding the Role of Hypoxia Inducible Factor During Neurodegeneration for New Therapeutics Opportunities.

Amalia Merelli, Julio César García Rodríguez, Jaume Folch, Marcelo R Regueiro, Antoni Camins, Alberto Lazarowski

Open access · bronzeAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025
    Pooled it
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  11. Hypoxia-inducible factor-1 as targets for neuroprotection : from ferroptosis to Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
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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 2 institutions in 3 countries.

Amalia MerelliINFIBIOC-FFyB-UBA-Buenos, Aires, Argentina.
Julio César García RodríguezCENPALAB. Biocubafarma; Havana, Cuba.
Jaume FolchDepartament de Bioquímica, Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, Spain.
Marcelo R RegueiroFellow of IMBS (International Master/PhD Program in Biomedical Sciences) University of Buenos Aires, Argentina and Freiburg University, Freiburg, Germany.
Antoni CaminsBiomedical Research Networking Center in Neurodegenerative Diseases (CIBERNED), Madrid, Spain.
Alberto LazarowskiINFIBIOC-FFyB-UBA-Buenos, Aires, Argentina.
Biomedical Research Networking Center on Neurodegenerative Diseases · ESUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegeneration (NDG) is linked with the progressive loss of neural function with intellectual and/or motor impairment. Several diseases affecting older individuals, including Alzheimer's disease, Amyotrophic Lateral Sclerosis, Huntington's disease, Parkinson's disease, stroke, Multiple Sclerosis and many others, are the most relevant disorders associated with NDG. Since other pathologies such as refractory epilepsy, brain infections, or hereditary diseases such as "neurodegeneration with brain iron accumulation", also lead to chronic brain inflammation with loss of neural cells, NDG can be said to affect all ages. Owing to an energy and/or oxygen supply imbalance, different signaling mechanisms including MAPK/PI3K-Akt signaling pathways, glutamatergic synapse formation, and/or translocation of phosphatidylserine, might activate some central executing mechanism common to all these pathologies and also related to oxidative stress. Hypoxia inducible factor 1-α (HIF-1α) plays a twofold role through gene activation, in the sense that this factor has to "choose" whether to protect or to kill the affected cells. Most of the afore-mentioned processes follow a protracted course and are accompanied by progressive iron accumulation in the brain. We hypothesize that the neuroprotective effects of iron chelators are acting against the generation of free radicals derived from iron, and also induce sufficient -but not excessive- activation of HIF-1α, so that only the hypoxia-rescue genes will be activated. In this regard, the expression of the erythropoietin receptor in hypoxic/inflammatory neurons could be the cellular "sign" to act upon by the nasal administration of pharmacological doses of Neuro-EPO, inducing not only neuroprotection, but eventually, neurorepair as well.

Indexed as

Drug DiscoveryAnimalsBrainCell HypoxiaErythropoietinHumansHypoxia-Inducible Factor 1, alpha SubunitIronIron Chelating AgentsNeurodegenerative DiseasesErythropoietinHypoxia-Inducible Factor 1, alpha SubunitIronIron Chelating AgentsHIF-1MDR-1NeurodegenerationNeuro-EPOneuroprotectionrefractory epilepsy.

Identifiers

PMID29318974
PMCPMC6295932
OpenAlexW2782597631

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.