Evidence map›Paper›PMID 41120204›Full record

ArticleJournal of biomedical research2025

The crosstalk between autophagy and ferroptosis in pulmonary fibrosis.

Rongzhu Liu, Dongnan Zheng, Fengxu Wang, Mengna Jiang, Rui Zhao, Shan Bao, Xinyuan Zhao, Demin Cheng

Abstract read
In one paragraph

Article in Journal of biomedical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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.

Rongzhu LiuDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.
Dongnan ZhengDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.
Fengxu WangDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.
Mengna JiangDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.
Rui ZhaoDepartment of Respiratory, Wuxi Eighth People's Hospital, Wuxi, Jiangsu 214000, China.
Shan BaoChina CDC Key Laboratory of Environment and Population Health, National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing 100021, China.
Xinyuan ZhaoDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.
Demin ChengDepartment of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu 226019, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is a progressive lung disorder characterized by excessive deposition of extracellular matrix (ECM) in the alveoli, with irreversible fibrotic remodeling and destruction of alveolar structures. Clinically, PF is manifested by progressive dyspnea and a decline in lung function. These manifestations contribute to a poor prognosis and significantly diminish the quality of life of affected individuals. Current therapeutic options for PF remain limited, highlighting the urgent need to elucidate its molecular mechanisms in order to develop novel treatment strategies. Recent studies have revealed that autophagy and ferroptosis, two critical cell death pathways, engage in intricate crosstalk mechanisms that regulate the pathogenesis of PF. Autophagy maintains cellular homeostasis by mediating lysosome-dependent degradation, whereas ferroptosis is characterized by iron-dependent lipid peroxidation. The interplay between autophagy and ferroptosis plays a pivotal role in modulating fibrosis progression. However, the mechanistic interactions between autophagy and ferroptosis in PF remain poorly understood, particularly regarding their bidirectional crosstalk and their unique role in PF progression. This review aims to systematically synthesize the current understanding of autophagy-ferroptosis interactions in PF, thereby identifying potential therapeutic strategies and drug targets for PF treatment.

Indexed as

autophagyferroptosispathogenic mechanismpulmonary fibrosistreatment strategies

Identifiers

PMID41120204
PMCPMC13620458

What OpenQuestion holds

Textmetadata
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.