Evidence map›Paper›PMID 32819193›Full record

ArticleStroke2020

Placental Mitochondria Therapy for Cerebral Ischemia-Reperfusion Injury in Mice.

Yoshihiko Nakamura, Eng H Lo, Kazuhide Hayakawa

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Pooled it
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  14. Causes of and Solutions to Mitochondrial Disorders: A Literature Review.International journal of molecular sciences · 2025
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4 more citing papers are in PubMed but not listed here.

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 1 country.

Yoshihiko NakamuraDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown.
Eng H LoDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown.
Kazuhide HayakawaDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown.
Massachusetts General Hospital · US

Funding

Promotion of neurovascular remodeling through mitochondria transfer after strokeR01NS094756 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HAYAKAWA, KAZUHIDE · 2015 to 2019
$1.9M
NINDS NIH HHS R01 NS094756
6 · The paper itself

Abstract

background and purposeThere is an urgent need to develop adjunct therapies that can be added onto reperfusion for acute ischemic stroke. Recently, mitochondrial transplantation has emerged as a promising therapeutic approach for boosting brain tissue protection. In this proof-of-concept study, we investigate the feasibility of using placenta as a source for mitochondrial transplantation in a mouse model of transient focal cerebral ischemia-reperfusion.

methodsMitochondria-enriched fractions were isolated from cryopreserved mouse placenta. Mitochondrial purity and JC1 membrane potentials were assessed by flow cytometry. Adenosine triphosphate and mitochondrial proteins were measured by luminescence intensity and western blot, respectively. Therapeutic efficacy of mitochondrial fractions was assessed in a mouse model of transient focal cerebral ischemia-reperfusion.

resultsFlow cytometry analysis demonstrated that about 87% of placental mitochondria were viable and maintained JC1 membrane potentials after isolation. Placental mitochondrial fractions contained adenosine triphosphate equivalent to mitochondrial fractions isolated from skeletal muscle and brown fat tissue. Normalized mitochondrial antioxidant enzymes (glutathione reductase, MnSOD [manganese superoxide dismutase]) and HSP70 (heat shock protein 70) were highly preserved in placental mitochondrial fractions. Treatment with placental mitochondrial fractions immediately after reperfusion significantly decreased infarction after focal cerebral ischemia in mice.

conclusionsCryopreserved placenta can be a feasible source for viable mitochondrial isolation. Transplantation with placental mitochondria may amplify beneficial effects of reperfusion in stroke.

Indexed as

AnimalsFemaleFlow CytometryGlutathione ReductaseHSP70 Heat-Shock ProteinsMembrane Potential, MitochondrialMiceMitochondriaPlacentaPregnancyReperfusion InjurySuperoxide DismutaseGlutathione ReductaseHSP70 Heat-Shock ProteinsSuperoxide Dismutasemembrane potentialsmitochondrial proteinsplacentaproof of concept studystroke

Identifiers

PMID32819193
PMCPMC7530055
OpenAlexW3080157062

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.