Evidence map›Paper›PMID 35563704›Full record

ReviewCells2022

The Role of Ferroptosis in Adverse Left Ventricular Remodeling Following Acute Myocardial Infarction.

Kyoko Komai, Nicholas K Kawasaki, Jason K Higa, Takashi Matsui

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
5.8field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Biomedicines · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 2 countries.

Kyoko KomaiDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI 96813, USA.
Nicholas K KawasakiDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI 96813, USA.
Jason K HigaDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI 96813, USA.ORCID 0000-0002-0429-6254
Takashi MatsuiDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI 96813, USA.
University of Hawaiʻi at Mānoa · US

Funding

TRPA1 Physiology in Diabetes, Metabolic Syndrome, and MetabolismP20GM113134 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI Michael A. Ortega · 2017 to 2026
$21.5M
Training in Cardiovascular Research at the University of HawaiiT32HL115505 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI Michelle D Tallquist · 2012 to 2026
$3.8M
NHLBI NIH HHS T32 HL115505NIGMS NIH HHS P20 GM113134
6 · The paper itself

Abstract

Ferroptosis is an iron-dependent form of regulated cell death and is distinct from other conventional forms of regulated cell death. It is often characterized by the dysfunction of the antioxidant selenoprotein glutathione peroxidase 4 (GPX4) antioxidant system. This loss of antioxidant capacity leads to the peroxidation of lipids and subsequent compromised plasma membrane structure. Disruption of the GPX4 antioxidant system has been associated with various conditions such as cardiomyopathy and ischemia-reperfusion (I/R) injury. GPX4 regulates lipid peroxidation, and chemical or genetic inhibition of GPX4 leads to reduced cardiac function. Iron chelators or antioxidants can be used for inhibiting ferroptosis, which restores functionality in in vivo and ex vivo experiments and confers overall cardioprotective effects against I/R injury. Moreover, suppression of ferroptosis also suppresses inflammation and limits the extent of left ventricle remodeling after I/R injury. Future research is necessary to understand the role of ferroptosis following an ischemic incident and can lead to the discovery of more potential therapeutics that prevent ferroptosis in the heart.

Indexed as

FerroptosisMyocardial InfarctionAntioxidantsHumansLipid PeroxidationVentricular RemodelingAntioxidantsferroptosisheartheart failureinflammationironLV remodelingmyocardial infarction

Identifiers

PMID35563704
PMCPMC9102292
OpenAlexW4224304468

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.