Evidence map›Paper›PMID 32385800›Full record

ArticleNeuromolecular medicine2020

Downregulation of Microrna-421 Relieves Cerebral Ischemia/Reperfusion Injuries: Involvement of Anti-apoptotic and Antioxidant Activities.

Yuehong Yue, Hongwei Zhao, Yuanyuan Yue, Yang Zhang, Wanyi Wei

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2020. 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
0.9field-weighted citation impact, top 32% 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, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Dexmedetomidine alleviates blood-brain barrier disruption in rats after cerebral ischemia-reperfusion by suppressing JNK and p38 MAPK signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  6. Article
  7. Review
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 1 institution in 1 country.

Yuehong YueDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050000, Hebei, People's Republic of China. dx3204@163.com.
Hongwei ZhaoDepartment of Gastroenterology, Hebei General Hospital, Shijiazhuang, 050000, Hebei, People's Republic of China.
Yuanyuan YueDepartment of Pharmacy, Hebei General Hospital, Shijiazhuang, 050000, Hebei, People's Republic of China.
Yang ZhangDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050000, Hebei, People's Republic of China.
Wanyi WeiDepartment of Neurology, Hebei General Hospital, Shijiazhuang, 050000, Hebei, People's Republic of China.
Hebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reperfusion after cerebral ischemia causes additional ischemic injuries due to sudden recovery of blood supply. It usually produces excessive reactive species, mitochondrial dysfunction, oxidative stress, and cell apoptosis. Our study is designed to examine the role of miR-421 antagomir in cerebral ischemia/reperfusion injuries, as well as its underlying mechanisms. Middle cerebral artery occlusion (MCAO) model was performed with male Sprague Dawley (SD) rats for the initiation of cerebral ischemia/reperfusion injuries. Malondialdehyde (oxidative stress marker) and superoxide dismutase (antioxidant enzyme) were measured as indicators for oxidative stress. Flow cytometry was utilized to evaluate the cell apoptosis effects from miR-421. miR-421 antagomir significantly decreased neurological deficits and infarction volumes. It also downregulated malondialdehyde contents, upregulated superoxide dismutase activities, promoted the expressions of myeloid cells leukemia-1 and B cells lymphoma-2, and downregulated the expressions of Bax in the ischemic cortex. In addition, miR-421targeted MCL1 to exert its biological functions. Our study indicated the neuroprotection effects of miR-421 antagomir on cerebral I/R injuries, which involved the suppression of cell apoptosis and oxidative stress. MiR-421 might provide a new therapeutic direction for ischemia/reperfusion injuries.

Indexed as

AnimalsAntagomirsAntioxidantsApoptosisApoptosis Regulatory ProteinsBrain IschemiaCerebral InfarctionDown-RegulationDrug Evaluation, PreclinicalGlutamic AcidInfarction, Middle Cerebral ArteryLipid PeroxidationMaleMalondialdehydeMyeloid Cell Leukemia Sequence 1 ProteinNeuroprotective AgentsAntagomirsAntioxidantsApoptosis Regulatory ProteinsGlutamic AcidMalondialdehydeMcl1 protein, ratMyeloid Cell Leukemia Sequence 1 ProteinNeuroprotective AgentsApoptosisIschemia/reperfusion injuriesMiddle cerebral artery occlusionMiR-421Oxidative stress

Identifiers

PMID32385800
OpenAlexW3023267686

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.