Evidence map›Paper›PMID 35309888›Full record

ArticleFrontiers in aging neuroscience2022

Neurons Release Injured Mitochondria as "Help-Me" Signaling After Ischemic Stroke.

Li Gao, Fan Liu, Pin-Pin Hou, Anatol Manaenko, Zhi-Peng Xiao, Fei Wang, Tian-Le Xu, Qin Hu

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  9. Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 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

8 authors.

Li GaoCentral Laboratory, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fan LiuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Pin-Pin HouCentral Laboratory, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Anatol ManaenkoDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhi-Peng XiaoCerebrovascular Disease Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fei WangCerebrovascular Disease Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tian-Le XuDepartment of Anatomy and Physiology, Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qin HuCentral Laboratory, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction has been regarded as one of the major contributors of ischemic neuronal death after stroke. Recently, intercellular mitochondrial transfer between different cell types has been widely studied and suggested as a potential therapeutic approach. However, whether mitochondria are involved in the neuron-glia cross-talk following ischemic stroke and the underlying mechanisms have not been explored yet. In this study, we demonstrated that under physiological condition, neurons release few mitochondria into the extracellular space, and the mitochondrial release increased when subjected to the challenges of acidosis, hydrogen peroxide (H

Indexed as

ischemic strokemetabolic stressmitochondrial biogenesismitochondrial releaseneuron-glial crosstalk

Identifiers

PMID35309888
PMCPMC8926840

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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.