Evidence map›Paper›PMID 31152363›Full record

ArticleNeuromolecular medicine2019

Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia.

Chinthasagar Bastian, Jerica Day, Stephen Politano, John Quinn, Sylvain Brunet, Selva Baltan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuromolecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Common methods in mitochondrial research (Review).International journal of molecular medicine · 2022
    Article
  3. Review
  4. Article
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.

Chinthasagar BastianDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA.
Jerica DayDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA.
Stephen PolitanoDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA.
John QuinnDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA.
Sylvain BrunetDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA.
Selva BaltanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue/NC30, Cleveland, OH, 44195, USA. baltans@ccf.org.ORCID http://orcid.org/0000-0003-1123-3582

Funding

Vulnerability of Aging White Matter to IschemiaR01AG033720 · NIA · UNIVERSITY OF WASHINGTON · PI BALTAN, SELVA · 2010 to 2021
$2.7M
Casein kinase 2 signaling in axonal injuryR21NS094881 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BALTAN, SELVA · 2016 to 2017
$436k
Vulnerability of Aging White Matter to IschemiaR56AG033720 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI BALTAN, SELVA · 2016 to 2016
$396k
NIA NIH HHS R01 AG033720NIA NIH HHS R56 AG033720NINDS NIH HHS R21 NS094881
6 · The paper itself

Abstract

Stroke significantly affects white matter in the brain by impairing axon function, which results in clinical deficits. Axonal mitochondria are highly dynamic and are transported via microtubules in the anterograde or retrograde direction, depending upon axonal energy demands. Recently, we reported that mitochondrial division inhibitor 1 (Mdivi-1) promotes axon function recovery by preventing mitochondrial fission only when applied during ischemia. Application of Mdivi-1 after injury failed to protect axon function. Interestingly, L-NIO, which is a NOS3 inhibitor, confers post-ischemic protection to axon function by attenuating mitochondrial fission and preserving mitochondrial motility via conserving levels of the microtubular adaptor protein Miro-2. We propose that preventing mitochondrial fission protects axon function during injury, but that restoration of mitochondrial motility is more important to promote axon function recovery after injury. Thus, Miro-2 may be a therapeutic molecular target for recovery following a stroke.

Indexed as

Axonal TransportMitochondrial DynamicsAdenosine TriphosphateAgingAnimalsAxonsCalciumDrug Evaluation, PreclinicalHumansHypoxia-Ischemia, BrainIschemic StrokeMiceMitochondriaMitochondrial ProteinsNitric Oxide Synthase Type IIIOrnithine3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAdenosine TriphosphateCalciumMitochondrial ProteinsN(G)-iminoethylornithineNitric Oxide Synthase Type IIINos3 protein, mouseOrnithineQuinazolinonesrho GTP-Binding ProteinsRHOT2 protein, humanIschemiaMiro-2MitochondriaMitochondrial dynamicsNOS3Stroke

Identifiers

PMID31152363
PMCPMC6884671

What OpenQuestion holds

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Registered trials

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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.