Evidence map›Paper›PMID 37580393›Full record

ReviewCell death & disease2023

The diversified role of mitochondria in ferroptosis in cancer.

Yu'e Liu, Shiping Lu, Lei-Lei Wu, Liang Yang, Lixue Yang, Jinghan Wang

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed
92.8field-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

257 citing papers in PubMed, 359 citations in OpenAlex.

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  13. Light-Inducible Bispecific DNAzymes Reveal Mitochondrial FeAngewandte Chemie (International ed. in English) · 2026
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197 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 4 institutions in 2 countries.

Yu'e Liu *Institute of Hepatobiliary and Pancreatic Surgery, Department of Hepatobiliary and Pancreatic Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Shiping Lu *Center for Translational Research in infection and Inflammation, School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Lei-Lei Wu *Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, 200433, Shanghai, China.ORCID 0000-0002-7417-6864
Liang YangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Ningbo University, Ningbo, 315010, China.
Lixue YangDepartment of Biliary Tract Surgery II, Eastern Hepatobiliary Surgery Hospital, Shanghai, 200438, China. ylx899@aliyun.com.
Jinghan WangInstitute of Hepatobiliary and Pancreatic Surgery, Department of Hepatobiliary and Pancreatic Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China. jinghanwang2023@126.com.ORCID 0000-0002-1755-3731
Ningbo University · CNShanghai East Hospital · CNTongji University · CNTulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a form of regulated cell death induced by iron-dependent lipid peroxidation, and it has been studied extensively since its discovery in 2012. Induced by iron overload and ROS accumulation, ferroptosis is modulated by various cellular metabolic and signaling pathways. The GSH-GPX4 pathway, the FSP1-CoQ10 pathway, the GCH1-BH4 pathway, the DHODH-CoQH2 system and the sex hormones suppress ferroptosis. Mitochondrial iron metabolism regulates ferroptosis and mitochondria also undergo a morphological change during ferroptosis, these changes include increased membrane density and reduced mitochondrial cristae. Moreover, mitochondrial energy metabolism changes during ferroptosis, the increased oxidative phosphorylation and ATP production rates lead to a decrease in the glycolysis rate. In addition, excessive oxidative stress induces irreversible damage to mitochondria, diminishing organelle integrity. ROS production, mitochondrial membrane potential, mitochondrial fusion and fission, and mitophagy also function in ferroptosis. Notably, some ferroptosis inhibitors target mitochondria. Ferroptosis is a major mechanism for cell death associated with the progression of cancer. Metastasis-prone or metastatic cancer cells are more susceptible to ferroptosis. Inducing ferroptosis in tumor cells shows very promising potential for treating drug-resistant cancers. In this review, we present a brief retrospect of the discovery and the characteristics of ferroptosis, then we discuss the regulation of ferroptosis and highlight the unique role played by mitochondria in the ferroptosis of cancer cells. Furthermore, we explain how ferroptosis functions as a double-edged sword as well as novel therapies aimed at selectively manipulating cell death for cancer eradication.

Indexed as

FerroptosisNeoplasmsIronMitochondriaOxidative StressReactive Oxygen SpeciesIronReactive Oxygen Species

Identifiers

PMID37580393
PMCPMC10425449
OpenAlexW4385801788

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.