Evidence map›Paper›PMID 39844858›Full record

ReviewFrontiers in neuroscience2024

The mitochondria as a potential therapeutic target in cerebral I/R injury.

Susu Fang, Wenzhou Huang, Xinhui Qu, Wen Chai

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

4 authors.

Susu Fang *The Second Department of Neurology, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China.
Wenzhou Huang *Department of Orthopedics, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Xinhui QuThe Second Department of Neurology, Jiangxi Provincial People's Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China.
Wen ChaiDepartment of Neurology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a major cause of mortality and disability worldwide. Among patients with ischemic stroke, the primary treatment goal is to reduce acute cerebral ischemic injury and limit the infarct size in a timely manner by ensuring effective cerebral reperfusion through the administration of either intravenous thrombolysis or endovascular therapy. However, reperfusion can induce neuronal death, known as cerebral reperfusion injury, for which effective therapies are lacking. Accumulating data supports a paradigm whereby cerebral ischemia/reperfusion (I/R) injury is coupled with impaired mitochondrial function, contributing to the pathogenesis of ischemic stroke. Herein, we review recent evidence demonstrating a heterogeneous mitochondrial response following cerebral I/R injury, placing a specific focus on mitochondrial protein modifications, reactive oxygen species, calcium (Ca

Indexed as

acetylationCa2+cerebral ischemia/reperfusion injury (CIRI)inflammationmitochondrial turnovermitochondrionROS

Identifiers

PMID39844858
PMCPMC11752919

What OpenQuestion holds

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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.