Evidence map›Paper›PMID 34650699›Full record

ArticleAmerican journal of translational research2021

Fraxetin attenuates ferroptosis in myocardial infarction via AKT/Nrf2/HO-1 signaling.

Yifei Xu, Haiyan Lin, Huan Wang, Jie Pang, Ying Zhou

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Fraxetin Targeting to Sortase A Decreases the Pathogenicity ofAnimals : an open access journal from MDPI · 2024
    Article
  7. Article
  8. Review
  9. The role of ferroptosis in neurodegenerative diseases.Frontiers in cellular neuroscience · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Can Polyphenols Inhibit Ferroptosis?Antioxidants (Basel, Switzerland) · 2022
    Review
  16. Roots ofEvidence-based complementary and alternative medicine : eCAM · 2022
    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

5 authors at 3 institutions in 1 country.

Yifei XuDepartment of Cardiology, First Affiliated Hospital of Zhejiang Chinese Medical University Hangzhou 310006, Zhejiang Province, China.
Haiyan LinDepartment of Cardiology, Ningbo Medical Center Lihuili Hospital Ningbo 315000, Zhejiang Province, China.
Huan WangDepartment of Cardiology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College Hangzhou 310014, Zhejiang Province, China.
Jie PangDepartment of Cardiology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College Hangzhou 310014, Zhejiang Province, China.
Ying ZhouDepartment of Cardiology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College Hangzhou 310014, Zhejiang Province, China.
Hangzhou Medical College · CNNingbo Medical Center Lihuili Hospital · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial infarction (MI) is the principal cause of mortality globally. Fraxetin (Fra) has anti-oxidative and anti-inflammatory properties. Nevertheless, the functional action of Fra in the progression of MI has never been elucidated.

methodThe

resultsFra treatment could reduce the infraction size and restrain ferroptosis in rats with MI. Moreover, Fra reduced the activity of serum LDH, the accumulation of iron and the MDA level, and increased GSH and glutathione peroxidase 4 (GPX4) in rats with MI. Furthermore, Fra protected H9C2 myocardial cells against OGD/R-induced ferroptosis by up-regulating HO-1. Moreover, Fra activated phosphorylation of AKT and Nrf2 nuclear accumulation in MI

conclusionFra attenuated MI-induced ferroptosis via AKT/Nrf2/HO-1 signaling, providing a potential therapeutic agent for MI.

Indexed as

AKTferroptosisfraxetinheme oxygenase-1Myocardial infarctionnuclear factor erythroid 2-related factor 2

Identifiers

PMID34650699
PMCPMC8507044
OpenAlexW3207018320

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.