Evidence map›Paper›PMID 33751318›Full record

ReviewApoptosis : an international journal on programmed cell death2021

New insights into targeting mitochondria in ischemic injury.

Jingjing Jia, Haiqiang Jin, Ding Nan, Weiwei Yu, Yining Huang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.1field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

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  9. circRNA-79530 regulates Twist-mediated mitochondrial damageEuropean journal of histochemistry : EJH · 2025
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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

5 authors at 2 institutions in 1 country.

Jingjing JiaDepartment of Neurology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, 100034, China.
Haiqiang JinDepartment of Neurology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, 100034, China.
Ding NanDepartment of Neurology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, 100034, China.
Weiwei YuDepartment of Neurology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, 100034, China.
Yining HuangDepartment of Neurology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, 100034, China. ynhuang@bjmu.edu.cn.
Peking University · CNPeking University First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is the leading cause of adult disability and death worldwide. Mitochondrial dysfunction has been recognized as a marker of neuronal death during ischemic stroke. Maintaining the function of mitochondria is important for improving the survival of neurons and maintaining neuronal function. Damaged mitochondria induce neuronal cell apoptosis by releasing reactive oxygen species (ROS) and pro-apoptotic factors. Mitochondrial fission and fusion processes and mitophagy are of great importance to mitochondrial quality control. This paper reviews the dynamic changes in mitochondria, the roles of mitochondria in different cell types, and related signaling pathways in ischemic stroke. This review describes in detail the role of mitochondria in the process of neuronal injury and protection in cerebral ischemia, and integrates neuroprotective drugs targeting mitochondria in recent years, which may provide a theoretical basis for the progress of treatment of ischemic stroke. The potential of mitochondrial-targeted therapy is also emphasized, which provides valuable insights for clinical research.

Indexed as

Brain IschemiaMitochondriaAnimalsApoptosisDrug Delivery SystemsHumansIschemiaMitochondrial DynamicsMitophagyNeuronsNeuroprotective AgentsReactive Oxygen SpeciesSignal TransductionStrokeNeuroprotective AgentsReactive Oxygen SpeciesIschemic strokeMitochondriaMitochondrial dynamicsMitophagyNeuroprotective drugsReactive oxygen species

Identifiers

PMID33751318
OpenAlexW3133534638

What OpenQuestion holds

Textmetadata
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.