Evidence map›Paper›PMID 34904402›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons in Mammals from Ischemia by Reducing Intracellular Calcium-Mediated Excitotoxicity.

Alexandra Chovsepian, Daniel Berchtold, Katarzyna Winek, Uta Mamrak, Inés Ramírez Álvarez, Yanina Dening, Dominika Golubczyk, Luis Weitbrecht, Claudia Dames, Marine Aillery and 9 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 16 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

19 authors at 6 institutions in 4 countries.

Alexandra ChovsepianDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian University Hospital, Nussbaumstrasse. 7, 80336, Munich, Germany.
Daniel BerchtoldDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.ORCID 0000-0002-7865-4157
Katarzyna WinekDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.ORCID 0000-0003-3085-9054
Uta MamrakLaboratory of Experimental Stroke Research, Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Feodor-Lynen-Strasse 17, 81377, Munich, Germany.
Inés Ramírez ÁlvarezDepartment of Neurology, Ludwig-Maximilian University Hospital, Marchioninstrasse. 15, 81377, Munich, Germany.
Yanina DeningDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian University Hospital, Nussbaumstrasse. 7, 80336, Munich, Germany.
Dominika GolubczykTi-com LLC, Trylinskiego 2, Olsztyn, 10-683, Poland.ORCID 0000-0001-5692-6329
Luis WeitbrechtDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.
Claudia DamesDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.
Marine AilleryDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.
Celia Fernandez-SanzDepartment of Neurology, Ludwig-Maximilian University Hospital, Marchioninstrasse. 15, 81377, Munich, Germany.ORCID 0000-0002-3437-7792
Zdzislaw GajewskiCenter for Translational Medicine, Warsaw University of Life Sciences, Warsaw, 02-787, Poland.
Marianne DieterichDepartment of Neurology, Ludwig-Maximilian University Hospital, Marchioninstrasse. 15, 81377, Munich, Germany.
Miroslaw JanowskiProgram in Image Guided Neurointerventions, Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland, Baltimore, MD, 21201, USA.
Peter FalkaiDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian University Hospital, Nussbaumstrasse. 7, 80336, Munich, Germany.ORCID 0000-0003-2873-8667
Piotr WalczakProgram in Image Guided Neurointerventions, Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland, Baltimore, MD, 21201, USA.ORCID 0000-0002-3733-3322
Nikolaus PlesnilaLaboratory of Experimental Stroke Research, Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Feodor-Lynen-Strasse 17, 81377, Munich, Germany.
Andreas MeiselDepartment of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117, Berlin, Germany.ORCID 0000-0001-7233-5342
Francisco Pan-MontojoDepartment of Psychiatry and Psychotherapy, Ludwig-Maximilian University Hospital, Nussbaumstrasse. 7, 80336, Munich, Germany.ORCID 0000-0002-1647-5196
Charité - Universitätsmedizin Berlin · DEMunich Cluster for Systems Neurology · DELudwig-Maximilians-Universität München · DEStroke Association · GBUniversity of Maryland, Baltimore · USWarsaw University of Life Sciences · PL

Funding

Deutsche Forschungsgemeinschaft EXC 2145 SyNergy - ID 390857198German Ministry for Economy and Energy EXIST-Forschungstransfer GLYMIPRO-FKZ03EFLBY173
6 · The paper itself

Abstract

Stroke is the second leading cause of death and disability worldwide. Current treatments, such as pharmacological thrombolysis or mechanical thrombectomy, reopen occluded arteries but do not protect against ischemia-induced damage that occurs before reperfusion or neuronal damage induced by ischemia/reperfusion. It has been shown that disrupting the conversion of glyoxal to glycolic acid (GA) results in a decreased tolerance to anhydrobiosis in Caenorhabditis elegans dauer larva and that GA itself can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study, the protective effect of GA is tested in different ischemia models, i.e., in commonly used stroke models in mice and swine. The results show that GA, given during reperfusion, strongly protects against ischemic damage and improves functional outcome. Evidence that GA exerts its effect by counteracting the glutamate-dependent increase in intracellular calcium during excitotoxicity is provided. These results suggest that GA treatment has the potential to reduce mortality and disability in stroke patients.

Indexed as

AnimalsBrain IschemiaCalciumDesiccationDisease Models, AnimalGlycolatesMaleMiceMice, Inbred C57BLNeuroprotectionNeuroprotective AgentsReperfusion InjurySwineCalciumGlycolatesglycolic acidNeuroprotective Agentsglutamate-dependent excitotoxicityischemia-reperfusion damageneuroprotectionStroke

Identifiers

PMID34904402
PMCPMC8811841
OpenAlexW4200106121

What OpenQuestion holds

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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.