Evidence map›Paper›PMID 29549824›Full record

ReviewRedox biology2018

Diverse roles of mitochondria in ischemic stroke.

Jenq-Lin Yang, Sujira Mukda, Shang-Der Chen

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
250citing papers in PubMed, 1 pooled it
14.5field-weighted citation impact, top 1% 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

250 citing papers in PubMed, 1 synthesis or guideline pooled it, 426 citations in OpenAlex.

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190 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 2 institutions in 2 countries.

Jenq-Lin YangInstitute for Translation Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, 123 Dapi Road, Kaohsiung 83301, Taiwan, ROC.
Sujira MukdaInstitute for Translation Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, 123 Dapi Road, Kaohsiung 83301, Taiwan, ROC; Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, 25/25 Phuttamonthon 4 Road, Salaya, Nakhon Pathom 73170, Thailand.
Shang-Der ChenInstitute for Translation Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, 123 Dapi Road, Kaohsiung 83301, Taiwan, ROC; Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, 123 Dapi Road, Kaohsiung 83301, Taiwan, ROC; College of Medicine, Chang Gung University, 259 Wenhua 1st Road, Taoyuan 33302, Taiwan, ROC. Electronic address: chensd@adm.cgmh.org.tw.
Kaohsiung Chang Gung Memorial Hospital · TWMahidol University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is the leading cause of adult disability and mortality in most developing and developed countries. The current best practices for patients with acute ischemic stroke include intravenous tissue plasminogen activator and endovascular thrombectomy for large-vessel occlusion to improve clinical outcomes. However, only a limited portion of patients receive thrombolytic therapy or endovascular treatment because the therapeutic time window after ischemic stroke is narrow. To address the current shortage of stroke management approaches, it is critical to identify new potential therapeutic targets. The mitochondrion is an often overlooked target for the clinical treatment of stroke. Early studies of mitochondria focused on their bioenergetic role; however, these organelles are now known to be important in a wide range of cellular functions and signaling events. This review aims to summarize the current knowledge on the mitochondrial molecular mechanisms underlying cerebral ischemia and involved in reactive oxygen species generation and scavenging, electron transport chain dysfunction, apoptosis, mitochondrial dynamics and biogenesis, and inflammation. A better understanding of the roles of mitochondria in ischemia-related neuronal death and protection may provide a rationale for the development of innovative therapeutic regimens for ischemic stroke and other stroke syndromes.

Indexed as

ApoptosisBrain IschemiaHumansMitochondriaMitochondrial DynamicsNeuronsReactive Oxygen SpeciesStrokeReactive Oxygen SpeciesApoptosisInflammationIschemic strokeMitochondriaMitochondrial biogenesisMitochondrial dynamicsMitophagy

Identifiers

PMID29549824
PMCPMC5854930
OpenAlexW2790012847

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.