Evidence map›Paper›PMID 41145737›Full record

ReviewCell biology and toxicology2025

Ferroptosis: molecular mechanisms, pathophysiology, and role in pediatric pulmonary diseases.

Junjie Ning, Lina Qiao

Abstract readReview
In one paragraph

Review in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Inhibition of the EP300/Notch Signaling Pathway Regulates Proliferation and Apoptosis in Oral Squamous Cell Carcinoma.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
    Article
  2. Hyperoxia and iron homeostasis in developing human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  3. Article
  4. Article
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

2 authors.

Junjie NingScientific Research Department, First People's Hospital of Zigong City, Sichuan Province, Zigong, 643000, China.
Lina QiaoDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China. qiaolina@scu.edu.cn.

Funding

National Key Research and Development Program of China 2021YFC2701700, 2021YFC2701704
6 · The paper itself

Abstract

Ferroptosis is a distinct form of programmed cell death characterized by iron-dependent oxidative stress and the accumulation of intracellular reactive oxygen species. This process involves multiple structural alterations, such as rupture of the outer mitochondrial membrane, reduced mitochondrial volume, and the decrease or disappearance of cristae. Additionally, ferroptosis is accompanied by iron overload and heightened lipid peroxidation (LPO). Although ferroptosis has been extensively investigated in various adult diseases, including infectious diseases, neurodegenerative disorders, cancers, and cardiovascular conditions, its role in pediatric respiratory diseases remains unclear. The molecular mechanisms of ferroptosis, particularly iron overload and LPO, are closely linked to the oxidative stress and inflammatory responses commonly observed in respiratory diseases. This review aims to summarize the fundamental processes and regulatory mechanisms of ferroptosis and to explore its potential relevance in pediatric respiratory diseases. By analyzing these mechanisms in depth, we can not only contribute to elucidating the pathophysiological features of pediatric respiratory illnesses but also provide novel insights and therapeutic targets for treatment strategies focusing on ferroptosis, offering new directions for clinical prevention and therapy in respiratory diseases.

Indexed as

FerroptosisLung DiseasesAnimalsChildHumansIronIron OverloadLipid PeroxidationMitochondriaOxidative StressReactive Oxygen SpeciesIronReactive Oxygen SpeciesFerroptosisGlutathione peroxidase 4Iron metabolismLipid peroxidationReactive oxygen species

Identifiers

PMID41145737
PMCPMC12559158

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.