Evidence map›Paper›PMID 35771293›Full record

ArticleCellular and molecular neurobiology2023

Oxygen-Glucose Deprivation Decreases the Motility and Length of Axonal Mitochondria in Cultured Dorsal Root Ganglion Cells of Rats.

Shin Kikuchi, Takayuki Kohno, Takashi Kojima, Haruyuki Tatsumi, Yuki Ohsaki, Takafumi Ninomiya

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 94% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Shin KikuchiDepartment of Anatomy 1, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan. ksin@sapmed.ac.jp.ORCID http://orcid.org/0000-0002-0401-195X
Takayuki KohnoDepartment of Cell Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan.ORCID http://orcid.org/0000-0002-1782-3578
Takashi KojimaDepartment of Cell Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan.
Haruyuki TatsumiDepartment of Anatomy 1, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan.
Yuki OhsakiDepartment of Anatomy 1, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan.ORCID http://orcid.org/0000-0002-8472-6962
Takafumi NinomiyaDepartment of Anatomy 1, Sapporo Medical University School of Medicine, West 17, South 1, Chuo-ku, Sapporo, Hokkaido, 060-8556, Japan.
Sapporo Medical University · JP

Funding

Japan Society for the Promotion of Science 15K01419Japan Society for the Promotion of Science 19K05736Japan Society for the Promotion of Science 19K07464Japan Society for the Promotion of Science 21K06733
6 · The paper itself

Abstract

Controlling axonal mitochondria is important for maintaining normal function of the neural network. Oxygen-glucose deprivation (OGD), a model used for mimicking ischemia, eventually induces neuronal cell death similar to axonal degeneration. Axonal mitochondria are disrupted during OGD-induced neural degeneration; however, the mechanism underlying mitochondrial dysfunction has not been completely understood. We focused on the dynamics of mitochondria in axons exposed to OGD; we observed that the number of motile mitochondria significantly reduced in 1 h following OGD exposure. In our observation, the decreased length of stationary mitochondria was affected by the following factors: first, the halt of motile mitochondria; second, the fission of longer stationary mitochondria; and third, a transformation from tubular to spherical shape in OGD-exposed axons. Motile mitochondria reduction preceded stationary mitochondria fragmentation in OGD exposure; these conditions induced the decrease of stationary mitochondria in three different ways. Our results suggest that mitochondrial morphological changes precede the axonal degeneration while ischemia-induced neurodegeneration.

Indexed as

GlucoseOxygenAnimalsAxonsCells, CulturedGanglia, SpinalMitochondriaRatsRats, Sprague-DawleyGlucoseOxygenAxonFissionMitochondriaOxygen–glucose deprivation (OGD)

Identifiers

PMID35771293
PMCPMC11414435
OpenAlexW4283737050

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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.