Evidence map›Paper›PMID 40858556›Full record

ReviewCell death discovery2025

Metabolic dysregulation in pulmonary fibrosis: insights into amino acid contributions and therapeutic potential.

Hongyu Zheng, Lei Zhang, Congjian Wang, Yi Wang, Chenxi Zeng

Abstract readReview
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026
    Review
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  9. The effect and mechanism of total alkaloids ofFrontiers in pharmacology · 2026
    Article
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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

5 authors.

Hongyu ZhengDepartment of Pulmonary and Critical Care Medicine, NHC Key Laboratory of Respiratory Diseases, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Lei ZhangDepartment of Pulmonary and Critical Care Medicine, NHC Key Laboratory of Respiratory Diseases, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0003-4296-3721
Congjian WangDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yi WangDepartment of Pulmonary and Critical Care Medicine, NHC Key Laboratory of Respiratory Diseases, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. wangyi@tjh.tjmu.edu.cn.
Chenxi ZengDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. zcx95@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0001-7189-8637

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82422003
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and life-threatening interstitial lung disease characterized by excessive extracellular matrix deposition and fibroblast activation. Emerging evidence suggests that amino acid metabolism plays a crucial role in the pathogenesis of pulmonary fibrosis. Key amino acids, including arginine, proline, and glutamine, contribute to the regulation of fibroblast activity and collagen synthesis, all of which are essential for fibrotic progression. Studies in experimental models of pulmonary fibrosis have demonstrated significant metabolic dysregulation, further highlighting its relevance in disease development. Moreover, targeting amino acid metabolism has emerged as a promising therapeutic strategy, with novel drugs and interventions designed to modulate metabolic pathways showing potential in preclinical and clinical studies. This review explores the intricate interplay between amino acid metabolism and pulmonary fibrosis, discusses its implications for disease progression, and evaluates the therapeutic prospects of metabolic interventions in IPF management. Understanding these metabolic mechanisms may pave the way for more effective and personalized treatment strategies for IPF.

Identifiers

PMID40858556
PMCPMC12381058

What OpenQuestion holds

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Registered trials

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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.