Evidence map›Paper›PMID 37272058›Full record

ReviewAutophagy2023

GPX4 in cell death, autophagy, and disease.

Yangchun Xie, Rui Kang, Daniel J Klionsky, Daolin Tang

Open access · hybridAbstract readReview
In one paragraph

Review in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 343 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
343citing papers in PubMed, 4 pooled it
126.1field-weighted citation impact, top 1% 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

343 citing papers in PubMed, 4 syntheses or guidelines pooled it, 488 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2026
    Review
  7. Ferroptosis in liver biology and diseases.Hepatology communications · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Supramolecular Degraders: An Emerging Paradigm in Targeted Protein Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Regulation of Glutathione Peroxidase 4 in Diabetic Retinopathy.International journal of molecular sciences · 2026
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

283 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Yangchun XieDepartment of Oncology, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Rui KangDepartment of Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Daniel J KlionskyLife Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-7828-8118
Daolin TangDepartment of Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0002-1903-6180
The University of Texas Southwestern Medical Center · USCentral South University · CNUniversity of Michigan · US

Funding

The mechanism and regulation of autophagyR35GM131919 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DANIEL J. KLIONSKY · 2019 to 2026
$6.4M
NIGMS NIH HHS R35 GM131919
6 · The paper itself

Abstract

Selenoprotein GPX4 (glutathione peroxidase 4), originally known as PHGPX (phospholipid hydroperoxide glutathione peroxidase), is the main oxidoreductase in the use of glutathione as a reducing agent in scavenging lipid peroxidation products. There are three GPX4 isoforms: cytosolic (cGPX4), mitochondrial (mGPX4), and nuclear (nGPX4), with distinct spatiotemporal expression patterns during embryonic development and adult life. In addition to inducing the main phenotype of ferroptosis, the loss of GPX4 can in some cells trigger apoptosis, necroptosis, pyroptosis, or parthanatos, which mediates or accelerates developmental defects, tissue damage, and sterile inflammation. The interaction of GPX4 with the autophagic degradation pathway further modulates cell fate in response to oxidative stress. Impaired GPX4 function is implicated in tumorigenesis, neurodegeneration, infertility, inflammation, immune disorders, and ischemia-reperfusion injury. Additionally, the R152H mutation in GPX4 can promote the development of Sedaghatian-type spinal metaphyseal dysplasia, a rare and fatal disease in newborns. Here, we discuss the roles of classical GPX4 functions as well as emerging GPX4-regulated processes in cell death, autophagy, and disease.

Indexed as

AutophagyInflammationCell DeathGlutathione PeroxidaseHumansPhospholipid Hydroperoxide Glutathione PeroxidaseGlutathione PeroxidasePhospholipid Hydroperoxide Glutathione Peroxidaseautophagycell deathLipid peroxidationoxidoreductase

Identifiers

PMID37272058
PMCPMC10472888
OpenAlexW4379376877

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.