Evidence map›Paper›PMID 32180078›Full record

ArticleInflammation2020

lncRNA ZFAS1 Improves Neuronal Injury and Inhibits Inflammation, Oxidative Stress, and Apoptosis by Sponging miR-582 and Upregulating NOS3 Expression in Cerebral Ischemia/Reperfusion Injury.

Yanyan Zhang, Yiping Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Association of NOS3 rs1799983 Polymorphism with Cognitive Function in Patients with First Episode Depression.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
  5. Article
  6. Review
  7. LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025
    Review
  8. Review
  9. Article
  10. The protective role of RACK1 in hepatic ischemia‒reperfusion injury-induced ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Yanyan ZhangThe First People's Hospital of Lianyungang, Lianyungang, Jiangsu Province, China.
Yiping ZhangTaizhou Third People's Hospital, Taizhou, Jiangsu province, China. YipingZ2019@163.com.
Taizhou People's Hospital · CNThe First People’s Hospital of Lianyungang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between lncRNAs and miRNAs was reported to be associated with cerebral ischemia reperfusion injury (CIRI). Besides, the lncRNA ZFAS1 was significantly downregulated in patients with ischemic stroke. However, the exact biological role of ZFAS1 and its mechanism in CIRI remain to be elucidated. The current study was designed to explore the protective effects of ZFAS1 on neuronal injury, inflammation, oxidative stress, and neuronal apoptosis in CIRI. ZFAS1 and miR-582-3p levels were assessed by RT-qPCR. Cerebral infarction was assessed by tetrazolium chloride (TTC) staining. Inflammation and oxidative stress were measured by ELISA and matched test kits. The apoptotic rate and apoptotic mediators in OGD/R-suffered PC12 cells were respectively detected by flow cytometry and western blot. NO production was measured by NO kit and western blot assay. The regulatory relationship between lncRNA ZFAS1 and miR-582-3p was analyzed using the luciferase reporter assay. ZFAS1 was downregulated in CIRI. ZFAS1 overexpression alleviated neurological function deficit and neuronal damage in a MCAO rat model. Besides, ZFAS1 upregulation or miR-582-3p downregulation could both inhibit the inflammation, oxidative stress, and apoptosis and enhance NO level in OGD/R-suffered PC12 cells. Reporter assay indicated that ZFAS1 served as a molecular sponge for miR-582-3p. In addition, ZFAS1 could negatively regulate miR-582-3p expression and release its effects in CIRI. Taken together, our study revealed that lncRNA ZFAS1 protected against neuronal damage and modulated the inflammation, oxidative stress, apoptosis, and NO level via regulating miR-582-3p in cerebral I/R injury. Therefore, lncRNA ZFAS1 might serve as a therapeutic application to suppress CIRI progression.

Indexed as

AnimalsApoptosisBrain IschemiaGene ExpressionHumansInflammationMaleMicroRNAsNeuronsNitric Oxide Synthase Type IIIOxidative StressPC12 CellsRatsRats, Sprague-DawleyReperfusion InjuryRNA, Long NoncodingMicroRNAsMIRN582 microRNA, humanNitric Oxide Synthase Type IIINos3 protein, ratRNA, Long NoncodingZFAS1 long non-coding RNA, humancerebral ischemia reperfusion injurylncRNA-ZFAS1miR-582NOS3

Identifiers

PMID32180078
OpenAlexW3011691105

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.