Evidence map›Paper›PMID 40780620›Full record

ReviewMolecules and cells2025

Iron metabolism dysregulation and ferroptosis: Emerging drivers in pulmonary fibrosis pathogenesis and therapy.

Yawen Jiang, Ligang Zhang, Yuandong Lin, Xiangxing Zhu, Tao Wang, Zhu Zhu, Yingshan Chen, Dongsheng Tang

Abstract readReview
In one paragraph

Review in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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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

8 authors.

Yawen JiangGene Editing Technology Center of Guangdong Province, School of Medicine, Foshan University, Foshan 528225, China; Guangdong GemPharmatech Co, Ltd, Foshan 528000, China. Electronic address: 15072758207@163.com.
Ligang ZhangGene Editing Technology Center of Guangdong Province, School of Medicine, Foshan University, Foshan 528225, China. Electronic address: lgzhang@fosu.edu.cn.
Yuandong LinGene Editing Technology Center of Guangdong Province, School of Medicine, Foshan University, Foshan 528225, China; Guangdong GemPharmatech Co, Ltd, Foshan 528000, China. Electronic address: linyuandong2000@163.com.
Xiangxing ZhuGene Editing Technology Center of Guangdong Province, School of Medicine, Foshan University, Foshan 528225, China. Electronic address: zhu_xiangxing@126.com.
Tao WangGuangdong GemPharmatech Co, Ltd, Foshan 528000, China. Electronic address: wangtao@gempharmatech.com.
Zhu ZhuGuangdong GemPharmatech Co, Ltd, Foshan 528000, China. Electronic address: zhuzhu@gempharmatech.com.
Yingshan ChenGuangdong GemPharmatech Co, Ltd, Foshan 528000, China. Electronic address: chenys@gempharmatech.com.
Dongsheng TangGene Editing Technology Center of Guangdong Province, School of Medicine, Foshan University, Foshan 528225, China. Electronic address: tangdsh@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is an iron-dependent and regulated form of cell death, characterized by lipid peroxidation and oxidative stress. The progressive development of pulmonary fibrosis (PF) is closely linked to the ferroptosis pathway. Although the underlying mechanisms remain incompletely defined, this field has drawn intense research attention. Notable progress has been made in identifying ferroptosis-related metabolic pathways and key targets during PF development. In this review, we first summarize the basic regulation of iron metabolism in the human lung, iron metabolic imbalance, and the activation of ferroptosis. Second, we focus on elaborating the mechanistic connections between ferroptosis and PF, encompassing the clinical features, pathological manifestations, and core pathogenic mechanisms of PF, as well as the interplay between ferroptosis and 3 specific cell types in PF: alveolar epithelial cells, macrophages, and fibroblasts. Third, the research progress in the pharmacotherapy of PF is categorized into 3 categories: drugs already approved for PF and those under clinical trials; ferroptosis-targeted therapeutic strategies, including inhibitors, natural compounds, gene therapy, and combination strategies. This review, grounded in key metabolic pathways and therapeutic targets, systematically explores the complex relationships among iron metabolic disorders, ferroptosis, and PF progression. Our aim is to provide a theoretical and practical foundation for ferroptosis-targeted PF treatment.

Indexed as

FerroptosisIronPulmonary FibrosisAlveolar Epithelial CellsFibroblastsHomeostasisHumansMacrophages, AlveolarMetabolic Networks and PathwaysIronFerroptosisIron metabolismPulmonary fibrosisTherapeutic strategies

Identifiers

PMID40780620
PMCPMC12475529

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.