Evidence map›Paper›PMID 35012442›Full record

ArticleBioengineered2022

Inhibition of Long non-coding RNA zinc finger antisense 1 improves functional recovery and angiogenesis after focal cerebral ischemia via microRNA-144-5p/fibroblast growth factor 7 axis.

Tong Li, Bai Ling Qing, Yan Deng, Xian Ting Que, Cheng Zhi Wang, Hua Wen Lu, Shao Hua Wang, Zi Jun Wang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 35% 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, 8 citations in OpenAlex.

  1. Article
  2. The Role of miR-144 in Inflammatory Diseases: A Review.Immunity, inflammation and disease · 2025
    Review
  3. Article
  4. Angiogenesis after ischemic stroke.Acta pharmacologica Sinica · 2023
    Review
  5. Article
  6. Article
  7. Arginine attenuates chronic mountain sickness in rats via microRNA-144-5p.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Tong LiDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Bai Ling QingDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Yan DengDepartment of Medical Records, Nanning Second People's Hospital, Nanning, GuangXi, China.
Xian Ting QueDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Cheng Zhi WangDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Hua Wen LuDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Shao Hua WangDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
Zi Jun WangDepartment of Neurology, Nanning Second People's Hospital, Nanning, GuangXi, China.
The Second Nanning People's Hospital · CNXian Yang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA zinc finger antisense 1 (ZFAS1) has been probed in cerebral ischemia, while the regulatory mechanism of ZFAS1 in focal cerebral ischemia (FCI) via binding to microRNA (miR)-144-5p remains rarely explored. This study aims to decipher the function of ZFAS1 on FCI via sponging miR-144-5p to modulate fibroblast growth factor 7 (FGF7). The focal cerebral ischemia rat model was established by occlusion of the middle cerebral artery (MCAO) Lentivirus vectors altering ZFAS1, miR-144-5p or FGF7 expression were injected into rats before MCAO. Then, ZFAS1, miR-144-5p, and FGF7 levels were detected, the inflammatory factor level, oxidative stress level, angiogenesis, neurological function injury and neuronal apoptosis were assessed. The binding relations among ZFAS1, miR-144-5p and FGF7 were validated. ZFAS1 and FGF7 expression was elevated, while miR-144-5p expression was reduced in FCI rats. Decreased ZFAS1 or FGF7 or enriched miR-144-5p repressed the inflammatory response, oxidative stress, neuronal apoptosis, while it improved angiogenesis, and neurological function recovery; while up-regulated ZFAS1 exerted opposite effects. The augmented miR-144-5p or silenced FGF7 reversed the effects of enriched ZFAS1. ZFAS1 sponged miR-144-5p that targeted FGF7. Inhibition of lncRNA ZFAS1 improves functional recovery and angiogenesis after FCI via miR-144-5p/FGF7 axis. This study provides novel therapeutic targets for FCI treatment.

Indexed as

AnimalsBrain IschemiaDisease Models, AnimalFibroblast Growth Factor 7Gene Expression RegulationMaleMicroRNAsOxidative StressRatsRNA, Long NoncodingFgf7 protein, ratFibroblast Growth Factor 7MicroRNAsMIRN144 microRNA, ratRNA, Long Noncodingangiogenesisfibroblast growth factor 7Focal cerebral ischemialong non-coding RNA zinc finger antisense 1microRNA-144-5pneurological function

Identifiers

PMID35012442
PMCPMC8805975
OpenAlexW4205283161

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.