Evidence map›Paper›PMID 32160513›Full record

ReviewCell chemical biology2020

Autophagy-Dependent Ferroptosis: Machinery and Regulation.

Jiao Liu, Feimei Kuang, Guido Kroemer, Daniel J Klionsky, Rui Kang, Daolin Tang

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell chemical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 483 papers.

0numbers the graph read from it
0cells of the map it votes in
483citing papers in PubMed
50.8field-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

483 citing papers in PubMed, 770 citations in OpenAlex.

  1. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
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423 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

6 authors at 5 institutions in 4 countries.

Jiao LiuThe Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510600, China.
Feimei KuangThe Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510600, China.
Guido KroemerUniversité Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France; Equipe 11 Labellisée Ligue Nationale Contre le Cancer, Centre de Recherche des Cordeliers, 75006 Paris, France; Institut National de la Santé et de la Recherche Médicale, U1138, Paris, France; Université Pierre et Marie Curie, 75006 Paris, France; Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, 94800 Villejuif, France; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, 75015 Paris, France; Department of Women's and Children's Health, Karolinska University Hospital, 17176 Stockholm, Sweden.
Daniel J KlionskyLife Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Daolin TangThe Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510600, China; Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: daolin.tang@utsouthwestern.edu.
Third Affiliated Hospital of Guangzhou Medical University · CNHôpital Européen · FRSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

The mechanism and regulation of autophagyR35GM131919 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DANIEL J. KLIONSKY · 2019 to 2026
$6.4M
Mechanisms of Ferroptotic Cancer Cell DeathR01CA229275 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2019 to 2024
$1.8M
EPA EP-C-16-014NCI NIH HHS R01 CA229275NIGMS NIH HHS R35 GM131919
6 · The paper itself

Abstract

Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved cellular process capable of degrading various biological molecules (e.g., protein, glycogen, lipids, DNA, and RNA) and organelles (e.g., mitochondria, endoplasmic reticulum [ER] ribosomes, lysosomes, and micronuclei) via the lysosomal pathway. Ferroptosis is a type of oxidative stress-dependent regulated cell death associated with iron accumulation and lipid peroxidation. The recently discovered role of autophagy, especially selective types of autophagy (e.g., ferritinophagy, lipophagy, clockophagy, and chaperone-mediated autophagy), in driving cells toward ferroptotic death motivated us to explore the functional interactions between metabolism, immunity, and cell death. Here, we describe types of selective autophagy and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis. We also summarize chemical modulators that are currently available for triggering or blocking autophagy-dependent ferroptosis and that may be developed for therapeutic interventions in human diseases.

Indexed as

AutophagyFerroptosisAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsClass III Phosphatidylinositol 3-KinasesHumansIronLipid PeroxidationMicrotubule-Associated ProteinsSignal TransductionAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsClass III Phosphatidylinositol 3-KinasesIronMicrotubule-Associated Proteinsautophagyferroptosisnetworkregulated cell deathselective autophagy

Identifiers

PMID32160513
PMCPMC7166192
OpenAlexW3012507702

What OpenQuestion holds

Textmetadata
LicenceTDM
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.