Evidence map›Paper›PMID 33922080›Full record

ArticleMetabolites2021

Butyrate Prevents TGF-β1-Induced Alveolar Myofibroblast Differentiation and Modulates Energy Metabolism.

Hyo Yeong Lee, Somi Nam, Mi Jeong Kim, Su Jung Kim, Sung Hoon Back, Hyun Ju Yoo

Open access · goldAbstract read
In one paragraph

Article in Metabolites, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Inter-Organ Communication in Pulmonary Fibrosis: Systemic Modifiers of a Lung-Centered Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Review
  5. Phytosynbiotic Containing Double-Layer MicroencapsulatedAnimals : an open access journal from MDPI · 2026
    Article
  6. Dose-dependent protective effects ofFrontiers in pharmacology · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024
    Review
  15. Cuproptosis-related gene CDKN2A as a molecular target for IPF diagnosis and therapeutics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Hyo Yeong LeeDepartment of Convergence Medicine, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Somi NamSchool of Biological Sciences, University of Ulsan, Ulsan 44610, Korea.
Mi Jeong KimSchool of Biological Sciences, University of Ulsan, Ulsan 44610, Korea.ORCID 0000-0003-1610-7649
Su Jung KimDepartment of Convergence Medicine, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.ORCID 0000-0001-5729-2129
Sung Hoon BackSchool of Biological Sciences, University of Ulsan, Ulsan 44610, Korea.
Hyun Ju YooDepartment of Convergence Medicine, Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.ORCID 0000-0003-2617-444X
Ulsan College · KRUniversity of Ulsan · KR

Funding

Asan Institute of Life Sciences, Asan Medical Centerl; National Research Foundation of Korea 2018IP0540; 2019IP0540;2020R1F1A1066088, S.H.B.;2019R1F1A1056286, H.J.Y.;2017M3A9G7072745, S.H.B.; 2014R1A6A1030318, S.H.B.
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a serious lung disease characterized by excessive collagen matrix deposition and extracellular remodeling. Signaling pathways mediated by fibrotic cytokine transforming growth factor β1 (TGF-β1) make important contributions to pulmonary fibrosis, but it remains unclear how TGF-β1 alters metabolism and modulates the activation and differentiation of pulmonary fibroblasts. We found that TGF-β1 lowers NADH and NADH/NAD levels, possibly due to changes in the TCA cycle, resulting in reductions in the ATP level and oxidative phosphorylation in pulmonary fibroblasts. In addition, we showed that butyrate (C4), a short chain fatty acid (SCFA), exhibits potent antifibrotic activity by inhibiting expression of fibrosis markers. Butyrate treatment inhibited mitochondrial elongation in TGF-β1-treated lung fibroblasts and increased the mitochondrial membrane potential (MMP). Consistent with the mitochondrial observations, butyrate significantly increased ADP, ATP, NADH, and NADH/NAD levels in TGF-β1-treated pulmonary fibroblasts. Collectively, our findings indicate that TGF-β1 induces changes in mitochondrial dynamics and energy metabolism during myofibroblast differentiation, and that these changes can be modulated by butyrate, which enhances mitochondrial function.

Indexed as

butyratemetabolitesmitochondriamyofibroblast differentiationpulmonary fibrosisshort chain fatty acidsTGF-β1

Identifiers

PMID33922080
PMCPMC8143476
OpenAlexW3155408299

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.