Evidence map›Paper›PMID 37610710›Full record

ArticleAging2023

miR-100-5p activation of the autophagy response through inhibiting the mTOR pathway and suppression of cerebral infarction progression in mice.

Xiaoyun Cao, Xiangjian Zhang, Junmin Chen, Qian Sun, Yufan Sun, Na Lin, Xiaoxia Liu

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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

7 authors at 3 institutions in 1 country.

Xiaoyun CaoNeurology Department, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
Xiangjian ZhangHebei Collaborative Innovation Center for Cardio- Cerebrovascular Disease, Shijiazhuang, China.
Junmin ChenNeurology Department, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Qian SunNeurology Department, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yufan SunInstitute of Clinical Medicine, Hebei Medical University, Shijiazhuang, China.
Na LinNeurology Department, Shijiazhuang Hua Yao Hospital, Shijiazhuang, China.
Xiaoxia LiuNeurology Department, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CNThird Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, the association between microRNAs (miRNAs) and autophagy in cerebral infarction (CI) has attracted increasingly more attention. The mammalian target of the rapamycin (mTOR) pathway is a key protein regulating the autophagy response. miR-100-5p can bind to the mTOR protein, but its role in CI remains unclear yet. This experiment aims to clarify the role of miR-100-5p in CI. Bioinformatics analysis was performed to screen differentiated expressed functional genes between CI tissue and normal tissue specimens.

Indexed as

Cerebral InfarctionMicroRNAsAnimalsApoptosisAutophagyAutophagy-Related ProteinsMammalsMiceTOR Serine-Threonine KinasesAutophagy-Related ProteinsMicroRNAsMirn100 microRNA, mouseTOR Serine-Threonine Kinasesapoptosisautophagycerebral infarction (CI)miR-100-5pmTOR

Identifiers

PMID37610710
PMCPMC10497003
OpenAlexW4386055935

What OpenQuestion holds

Textmetadata
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.