Commentary: Can astrocytic mitochondria therapy be used as antioxidant conditioning to protect neurons?

Kazuhide Hayakawa

Open access · greenAbstract read

In one paragraph

Article in Conditioning medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact, top 70% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

Neuron-Glia Crosstalk in the Regulation of Astrocytic Antioxidative Mechanisms Following CNS Injury.Antioxidants (Basel, Switzerland) · 2025
Review

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

1 author at 1 institution in 1 country.

Kazuhide HayakawaNeuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA.

Massachusetts General Hospital · US

Funding

Extracellular Mitochondria Transfer in Gray and White Matter for Ameliorating Sensorimotor and Cognitive Deficits After StrokeR01NS126280 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI Kazuhide Hayakawa · 2022 to 2026

$2.5M

NINDS NIH HHS R01 NS126280

6 · The paper itself

Abstract

In the context of central nervous system (CNS) disease, oxidative stress may cause progression of cell death and neuroinflammation. Therefore, restoring mitochondrial antioxidant ability within cells is a major therapeutic strategy in many CNS disorders. A recent study uncovers a novel mechanism of astrocytic mitochondria being neuroprotective after intracerebral hemorrhage in mice. In their work, systemic administration of mitochondria obtained from astrocytes restores neuronal antioxidant defense, prevents neuronal death while promoting neurite outgrowth, indicating that extracellular mitochondria may play key roles in mediating beneficial non-cell autonomous effects. Given that mitochondria are also responsible for tolerance to stress and injury, is it possible that exogenous mitochondria signals may regulate cellular conditioning by boosting antioxidant ability? Further studies are warranted to build on these emerging findings in the pursuit of conditioning therapies mediated by mitochondrial transplantation in CNS injury and disease.

Indexed as

Antioxidant defenseAstrocytic mitochondriaCNS disordersMitochondrial transplantation

Identifiers

PMID38037662

PMCPMC10688760

OpenAlexW4389244229

What OpenQuestion holds

Textmetadata

LicenceTDM

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.