Evidence map›Paper›PMID 42045225›Full record

ArticleNature communications2026

Dietary intake and BCAA metabolism regulate pulmonary fibrosis through KDM4A-mediated epigenetic remodeling in male mice.

Jie Yao, Su Fang, Miao Lei, Zexian Ou, Chuanfei Zeng, Wanli Peng, Na He, Lian Yang, Bingpeng Guo, Mingmeng Fang and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

22 authors.

Jie Yao *GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou National Laboratory, Guangzhou Medical University, Guangzhou, China.
Su Fang *Guangzhou National Laboratory, Guangzhou, China.
Miao Lei *Guangzhou National Laboratory, Guangzhou, China.
Zexian OuGuangzhou National Laboratory, Guangzhou, China.ORCID http://orcid.org/0009-0002-7495-6905
Chuanfei ZengGuangzhou National Laboratory, Guangzhou, China.
Wanli PengGMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou National Laboratory, Guangzhou Medical University, Guangzhou, China.
Na HeGMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou National Laboratory, Guangzhou Medical University, Guangzhou, China.
Lian YangGuangzhou National Laboratory, Guangzhou, China.
Bingpeng GuoState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.
Mingmeng FangGuangzhou National Laboratory, Guangzhou, China.
Cuihua WangGuangzhou National Laboratory, Guangzhou, China.
Jie LvCancer Research Institute, School of Basic Medical Sciences, State Key Laboratory of Multi-organ Injury Prevention and Treatment, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, Southern Medical University, Guangzhou, China.
Shuang WuGuangzhou National Laboratory, Guangzhou, China.
Wei Kevin ZhangGuangzhou National Laboratory, Guangzhou, China.ORCID http://orcid.org/0000-0003-4960-6137
Huimin HuangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yang PengState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-2113-5858
Wei RaoKey Laboratory of Respiratory Disease of Zhejiang Province, Department of Respiratory and Critical Care Medicine of the Second Affiliated Hospital, Center for Stem Cell and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Zhili RongCancer Research Institute, School of Basic Medical Sciences, State Key Laboratory of Multi-organ Injury Prevention and Treatment, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-1699-7074
Penghui YangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.
Chaoqun WangZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, China.ORCID http://orcid.org/0000-0003-0415-6080
Qian HanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China. hanqian1020@yahoo.com.
Wenxiang HuGMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macau Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou National Laboratory, Guangzhou Medical University, Guangzhou, China. hu_wenxiang@gzlab.ac.cn.ORCID http://orcid.org/0000-0002-6754-5625

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82270868, 82204682
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis is a progressive and fatal disorder characterized by abnormal activation of alveolar fibroblasts. However, the metabolic reprogramming of alveolar fibroblasts during lung injury remains unclear. Here we show that uptake of branched-chain amino acids is increased, whereas their catabolism is significantly impaired in fibrotic lung fibroblasts and mouse lung tissues. Branched-chain amino acids promote lung fibroblast activation and bleomycin-induced lung fibrosis. Genetic inactivation of branched-chain amino acid transaminase 2 exacerbates fibrosis, whereas inhibition of the corresponding transporter SLC7A5 or enhancement of catabolism attenuates pulmonary fibrosis in male mice. Mechanistically, ATF4 and PPARγ regulate the expression of SLC7A5 and BCAA catabolic genes, respectively. We identify KDM4A as a key mediator of the epigenetic regulation of fibrotic genes. Notably, dysregulated BCAA metabolism is associated with disease severity in patients, suggesting that targeting BCAA metabolism may serve as a promising therapeutic strategy for idiopathic pulmonary fibrosis.

Indexed as

Amino Acids, Branched-ChainEpigenesis, GeneticIdiopathic Pulmonary FibrosisJumonji Domain-Containing Histone DemethylasesPulmonary FibrosisActivating Transcription Factor 4AnimalsBleomycinDietDisease Models, AnimalFibroblastsHumansLungMaleMiceMice, Inbred C57BLActivating Transcription Factor 4Amino Acids, Branched-ChainBleomycinJumonji Domain-Containing Histone DemethylasesPPAR gammaTransaminases

Identifiers

PMID42045225
PMCPMC13324639

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.