Evidence map›Paper›PMID 35422492›Full record

ReviewCell death and differentiation2022

Non-coding RNAs and ferroptosis: potential implications for cancer therapy.

Amar Balihodzic, Felix Prinz, Michael A Dengler, George A Calin, Philipp J Jost, Martin Pichler

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
17.4field-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

91 citing papers in PubMed, 180 citations in OpenAlex.

  1. Review
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  4. MiR-940 Suppresses Ferroptosis by Controlling Expression of Key Regulatory Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  11. Macrophage ferroptosis in hematologic malignancies: emerging mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
    Review
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31 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 2 institutions in 3 countries.

Amar BalihodzicDepartment of Internal Medicine, Division of Oncology, Medical University of Graz, 8036, Graz, Austria.ORCID http://orcid.org/0000-0002-1568-6784
Felix PrinzDepartment of Internal Medicine, Division of Oncology, Medical University of Graz, 8036, Graz, Austria.
Michael A DenglerDepartment of Internal Medicine, Division of Oncology, Medical University of Graz, 8036, Graz, Austria.ORCID http://orcid.org/0000-0002-1693-1761
George A CalinDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.ORCID http://orcid.org/0000-0002-7427-0578
Philipp J JostDepartment of Internal Medicine, Division of Oncology, Medical University of Graz, 8036, Graz, Austria.
Martin PichlerDepartment of Internal Medicine, Division of Oncology, Medical University of Graz, 8036, Graz, Austria. martin.pichler@medunigraz.at.ORCID http://orcid.org/0000-0002-8701-9462
Medical University of Graz · ATThe University of Texas MD Anderson Cancer Center · US

Funding

Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

Ferroptosis is a recently defined form of regulated cell death, which is biochemically and morphologically distinct from traditional forms of programmed cell death such as apoptosis or necrosis. It is driven by iron, reactive oxygen species, and phospholipids that are oxidatively damaged, ultimately resulting in mitochondrial damage and breakdown of membrane integrity. Numerous cellular signaling pathways and molecules are involved in the regulation of ferroptosis, including enzymes that control the cellular redox status. Alterations in the ferroptosis-regulating network can contribute to the development of various diseases, including cancer. Evidence suggests that ferroptosis is commonly suppressed in cancer cells, allowing them to survive and progress. However, cancer cells which are resistant to common chemotherapeutic drugs seem to be highly susceptible to ferroptosis inducers, highlighting the great potential of pharmacologic modulation of ferroptosis for cancer treatment. Non-coding RNAs (ncRNAs) are considered master regulators of various cellular processes, particularly in cancer where they have been implicated in all hallmarks of cancer. Recent work also demonstrated their involvement in the molecular control of ferroptosis. Hence, ncRNA-based therapeutics represent an exciting alternative to modulate ferroptosis for cancer therapy. This review summarizes the ncRNAs implicated in the regulation of ferroptosis in cancer and highlights their underlying molecular mechanisms in the light of potential therapeutic applications.

Indexed as

FerroptosisNeoplasmsApoptosisCell DeathHumansOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID35422492
PMCPMC9177660
OpenAlexW4223969900

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.