Evidence map›Paper›PMID 33723216›Full record

ArticleCell death & disease2021

MiR-127-3p targeting CISD1 regulates autophagy in hypoxic-ischemic cortex.

Zi-Bin Zhang, Liu-Lin Xiong, Lu-Lu Xue, Yan-Ping Deng, Ruo-Lan Du, Qiao Hu, Yang Xu, Si-Jin Yang, Ting-Hua Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Zi-Bin Zhang *Institute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Liu-Lin Xiong *Institute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Lu-Lu XueAnimal Zoology Department, Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, 650500, China.
Yan-Ping DengNational Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research Center, Department of Anaesthesiology, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, China.
Ruo-Lan DuInstitute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Qiao HuInstitute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yang XuInstitute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Si-Jin YangNational Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research Center, Department of Anaesthesiology, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, China. ysjimn@sina.com.
Ting-Hua WangInstitute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, China. Wangth_email@163.com.
Sichuan University · CNKunming Medical University · CNSouthwest Medical University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal hypoxic-ischemic (HI) injury derived from asphyxia during perinatal period, is a serious complication of neonatal asphyxia and the main cause of neonatal acute death and chronic neurological injury. Aberrant autophagy occurs in many nervous system diseases, but its role and underlying mechanism in HI injury is largely unknown. Here, we successfully constructed a newborn rat model of HI brain injury, and the knockout-miR-127-3p (KO-miR-127-3p) rats were structured by using CRISPR/Cas9. Subsequently, the in vitro functional experiments, in vivo zea-longa scores, as well as bioinformatics analyses and biological experiments were applied. The expression of autophagy-related proteins, including ATG12, P62, Beclin-1, LC3II in HI cortex with miR-127-3p knockout was significantly decreased, and autophagic vacuoles were disappeared. Moreover, miR-127-3p has a specific regulatory effect on CISD1 expression, another crucial molecule in autophagy process. Accordingly, the overexpression of CISD1 effectively inhibited the autophagic cell death and physiological dysfunction in the brain of HI injury, whereas si-CISD1 reversed the neuroprotective effects of KO-miR-127-3p. Our findings explained the underlying mechanism for HI injury, and miR-127-3p targeting CISD1 signal could be supposed as a new treatment strategy to prevent and treat HI injury.

Indexed as

AutophagyAnimalsAnimals, NewbornAutophagy-Related ProteinsCerebral CortexDisease Models, AnimalFemaleHypoxia-Ischemia, BrainMaleMicroRNAsMitochondriaNeuronsPC12 CellsRatsRats, Sprague-DawleyRats, TransgenicAutophagy-Related ProteinsMicroRNAsMirn127 microRNA, rat

Identifiers

PMID33723216
PMCPMC7961148
OpenAlexW3139132666

What OpenQuestion holds

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LicenceCC BY
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.