Evidence map›Paper›PMID 33578870›Full record

ReviewCells2021

Endogenous Mechanisms of Neuroprotection: To Boost or Not to Boost.

Sara Marmolejo-Martínez-Artesero, Caty Casas, David Romeo-Guitart

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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

3 authors at 1 institution in 2 countries.

Sara Marmolejo-Martínez-ArteseroDepartment of Cell Biology, Physiology and Immunology, Institut de Neurociències (INc), Universitat Autònoma de Barcelona (UAB), Bellaterra, 08193 Barcelona, Spain.ORCID 0000-0001-5357-2123
Caty CasasDepartment of Cell Biology, Physiology and Immunology, Institut de Neurociències (INc), Universitat Autònoma de Barcelona (UAB), Bellaterra, 08193 Barcelona, Spain.ORCID 0000-0002-2273-6321
David Romeo-GuitartDepartment of Cell Biology, Physiology and Immunology, Institut de Neurociències (INc), Universitat Autònoma de Barcelona (UAB), Bellaterra, 08193 Barcelona, Spain.
Universitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postmitotic cells, like neurons, must live through a lifetime. For this reason, organisms/cells have evolved with self-repair mechanisms that allow them to have a long life. The discovery workflow of neuroprotectors during the last years has focused on blocking the pathophysiological mechanisms that lead to neuronal loss in neurodegeneration. Unfortunately, only a few strategies from these studies were able to slow down or prevent neurodegeneration. There is compelling evidence demonstrating that endorsing the self-healing mechanisms that organisms/cells endogenously have, commonly referred to as cellular resilience, can arm neurons and promote their self-healing. Although enhancing these mechanisms has not yet received sufficient attention, these pathways open up new therapeutic avenues to prevent neuronal death and ameliorate neurodegeneration. Here, we highlight the main endogenous mechanisms of protection and describe their role in promoting neuron survival during neurodegeneration.

Indexed as

NeuroprotectionAnimalsApoptosisAutophagyCaloric RestrictionHumansNeuroprotective AgentsUnfolded Protein ResponseNeuroprotective Agentsautophagycellular resilienceendogenous mechanismsneuronal survivalneuroprotectionunfolded protein response

Identifiers

PMID33578870
PMCPMC7916582
OpenAlexW3128163600

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.