Evidence map›Paper›PMID 24008571›Full record

ArticleStroke2013

Ischemic stroke brain sends indirect cell death signals to the heart.

Hiroto Ishikawa, Naoki Tajiri, Julie Vasconcellos, Yuji Kaneko, Osamu Mimura, Mari Dezawa, Cesar V Borlongan

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. NF-Frontiers in cardiovascular medicine · 2026
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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

7 authors at 2 institutions in 1 country.

Hiroto IshikawaFrom the Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL (H.I., N.T., J.V., Y.K., C.V.B.); Department of Ophthalmology, Hyogo College of Medicine, Nishinomiya, Japan (H.I., O.M.); and Department of Stem Cell Biology and Histology and Department of Anatomy and Anthropology, Tohoku University Graduate School of Medicine, Sendai, Japan (M.D.).
Naoki Tajiri
Julie Vasconcellos
Yuji Kaneko
Osamu Mimura
Mari Dezawa
Cesar V Borlongan
Hyogo Medical University · JPTohoku University · JP

Funding

Blood-Brain Barrier Repair in Cell Therapy for StrokeR01NS071956 · NINDS · UNIVERSITY OF SOUTH FLORIDA · PI BORLONGAN, CESARIO V, GARBUZOVA-DAVIS, SVITLANA NICOLAI · 2011 to 2015
$2.1M
NINDS NIH HHS 1R01NS071956-01NINDS NIH HHS R01 NS071956
6 · The paper itself

Abstract

background and purposeIschemic stroke is a leading cause of mortality and morbidity in the world and may be associated with cardiac myocyte vulnerability. However, it remains uncertain how an ischemic brain contributes to cardiac alternations. Here, we used experimental stroke models to reveal the pathological effects of the ischemic brain on the heart.

methodsFor the in vitro study, primary rat neuronal cells were subjected to 90-minute oxygen-glucose deprivation (OGD). Two hours after OGD, the supernatant was collected and cryopreserved until further biological assays. Primary rat cardiac myocytes were exposed to ischemic-reperfusion injury and subsequently to the supernatant derived from either the OGD or non-OGD-exposed primary rat neuronal cells for 2, 6, 24, or 48 hours. Thereafter, we measured cell viability and mitochondrial activity in rat cardiac myocytes. For the in vivo study, we subjected adult rats to transient middle cerebral artery occlusion, and their brains and hearts were harvested for immunohistochemical analyses at 3 months later.

resultsThe supernatant from the OGD, but not the non-OGD-exposed primary rat neuronal cells, caused significant reduction in cell viability and mitochondrial activity in rat cardiac myocytes. Ischemic stroke animals displayed phenotypic expression of necrosis, apoptosis, and autophagy in their hearts, which paralleled the detection of these same cell death markers in their brains.

conclusionsIschemic stroke was accompanied by cardiac myocyte death, indicating a close pathological link between brain and heart. These results suggest a vigilant assessment of the heart condition in stroke patients, likely requiring the need to treat systemic cardiac symptoms after an ischemic brain episode.

Indexed as

ApoptosisAutophagyAnimalsBrain IschemiaCells, CulturedCell SurvivalGlucoseMitochondriaMyocardiumMyocytes, CardiacNecrosisNeuronsOxygenRatsReperfusion InjuryRisk FactorsGlucoseOxygenapoptosisautophagybrain ischemiamyocytes, cardiacnecrosis

Identifiers

PMID24008571
PMCPMC3859251
OpenAlexW2152141631

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.