Evidence map›Paper›PMID 39721015›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Fatty Acid Oxidation-Glycolysis Metabolic Transition Affects ECM Homeostasis in Silica-Induced Pulmonary Fibrosis.

Wenqing Sun, Siyun Zhou, Lan Peng, Wei Wang, Yi Liu, Ting Wang, Demin Cheng, Ziwei Li, Haojie Xiong, Xinying Jia and 3 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Tools of the trade: leveraging 3DFrontiers in pharmacology · 2026
    Review
  17. Article
  18. Article
  19. Review
  20. 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

13 authors.

Wenqing SunThe Affiliated Wuxi Center for Disease Control and Prevention of Nanjing Medical University, Wuxi Center for Disease Control and Prevention, Wuxi Medical Center, Nanjing medical university, Nanjing, 211166, China.
Siyun ZhouDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Lan PengDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Wei WangThe Affiliated Wuxi Center for Disease Control and Prevention of Nanjing Medical University, Wuxi Center for Disease Control and Prevention, Wuxi Medical Center, Nanjing medical university, Nanjing, 211166, China.
Yi LiuDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Ting WangDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Demin ChengDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Ziwei LiDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Haojie XiongDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Xinying JiaDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Wenxiu LianDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Jiandong JiaoThe Affiliated Wuxi Center for Disease Control and Prevention of Nanjing Medical University, Wuxi Center for Disease Control and Prevention, Wuxi Medical Center, Nanjing medical university, Nanjing, 211166, China.
Chunhui NiDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.ORCID https://orcid.org/0000-0002-6539-2434

Funding

National Natural Science Foundation of China 82073518Top Talent Support Program for Young and Middle-aged People HB2023099
6 · The paper itself

Abstract

Silicosis is a fatal occupational pulmonary disease that is characterized by irreversible replacement of lung parenchyma by aberrant Exracellular matrix (ECM). Metabolic reprogramming is a crucial mechanism for fibrosis. However, how the metabolic rewiring shifts the ECM homeostasis toward overaccumulation remains unclear. Herein, a phenotype with reduction in fatty acid oxidation (FAO) but enhanced glycolysis in myofibroblasts is shown. Perturbation of the glycolytic and FAO pathways, respectively, reveals distinct roles in the metabolic distribution of ECM deposition and degradation. Suppressed glycolysis leads to a decrease in insoluble ECM, primarily due to the inhibition of ECM-modifying enzyme activity and a decrease in glycine synthesis. Notably, promoted FAO facilitates the intracellular degradation pathway of ECM. In addition, the findings revealed that hypoxia-inducible factor-1 alpha (HIF-1α) serves as a crucial metabolic regulator in the transition from FAO to glycolysis, thereby playing a significant role in ECM deposition in silica-induced pulmonary fibrosis. Further, the promotion of FAO, inhibition of glycolysis and HIF-1α reduce ECM production and promote ECM degradation, ultimately impeding the progression of fibrosis and providing therapeutic relief for established pulmonary fibrosis in vivo. These findings unveil the metabolic rewire underpinning the deposition of ECM in silica-induced lung fibrosis and identify novel targets for promoting regression of pulmonary fibrosis.

Indexed as

Extracellular MatrixFatty AcidsGlycolysisPulmonary FibrosisSilicon DioxideAnimalsHomeostasisHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLMyofibroblastsOxidation-ReductionSilicosisFatty AcidsHypoxia-Inducible Factor 1, alpha SubunitSilicon Dioxideextracellular matrixfatty acid oxidationglycolysishypoxia‐inducible factor‐1αsilicosis

Identifiers

PMID39721015
PMCPMC11831484

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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.