Evidence map›Paper›PMID 39122680›Full record

ArticleCell death & disease2024

CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.

Hua Ni, Miao Chen, Dan Dong, Yunqiang Zhou, Yu Cao, Ruixin Ge, Xiangrui Luo, Yutao Wang, Xifeng Dong, Jun Zhou and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. 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. Review
  2. Review
  3. Article
  4. Role of HDAC6 in carcinomas.Discover oncology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Article
  12. Frontiers in microbiology · 2025
    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.

Hua Ni *State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Miao Chen *School of Life Sciences and Medicine, Shandong University of Technology, Zibo, China.
Dan Dong *State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Yunqiang ZhouState Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Yu CaoCenter for Cell Structure and Function, Collaborative Innovation Center of Cell Biology in Universities of Shandong, College of Life Sciences, Shandong Normal University, Jinan, China.
Ruixin GeCenter for Cell Structure and Function, Collaborative Innovation Center of Cell Biology in Universities of Shandong, College of Life Sciences, Shandong Normal University, Jinan, China.
Xiangrui LuoCenter for Cell Structure and Function, Collaborative Innovation Center of Cell Biology in Universities of Shandong, College of Life Sciences, Shandong Normal University, Jinan, China.
Yutao WangKey Laboratory of Biological Resources and Ecology of Pamirs Plateau in Xinjiang Uygur Autonomous Region, College of Life and Geographic Sciences, Kashi University, Kashi, China.
Xifeng DongDepartment of Hematology, Tianjin Key Laboratory of Bone Marrow Failure and Malignant Hemopoietic Clone Control, Tianjin Institute of Hematology, Tianjin Medical University General Hospital, Tianjin, China.
Jun ZhouState Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.ORCID 0000-0001-7858-8260
Dengwen LiState Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China. dwli@nankai.edu.cn.ORCID 0000-0002-4573-7191
Songbo XieDepartment of Ophthalmology, Tianjin Medical University General Hospital, Ministry of Education International Joint Laboratory of Ocular Diseases, Tianjin Key Laboratory of Ocular Trauma, Tianjin Institute of Eye Health and Eye Diseases, China-UK "Belt and Road" Ophthalmology Joint Laboratory, Haihe Laboratory of Cell Ecosystem, Tianjin Medical University, Tianjin, 300052, China. songboxie@tmu.edu.cn.ORCID 0000-0003-3195-6948
Min LiuLaboratory of Tissue Homeostasis, Haihe Laboratory of Cell Ecosystem, Tianjin, China. minliu@nankai.edu.cn.ORCID 0009-0003-8010-3084

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32070708National Natural Science Foundation of China (National Science Foundation of China) 32170829National Natural Science Foundation of China (National Science Foundation of China) 32270892National Natural Science Foundation of China (National Science Foundation of China) 82072256
6 · The paper itself

Abstract

The primary cilium behaves as a platform for sensing and integrating extracellular cues to control a plethora of cellular activities. However, the functional interaction of this sensory organelle with epithelial-mesenchymal transition (EMT) during pulmonary fibrosis remains unclear. Here, we reveal a critical role for cylindromatosis (CYLD) in reciprocally linking the EMT program and ciliary homeostasis during pulmonary fibrosis. A close correlation between the EMT program and primary cilia is observed in bleomycin-induced pulmonary fibrosis as well as TGF-β-induced EMT model. Mechanistic study reveals that downregulation of CYLD underlies the crosstalk between EMT and ciliary homeostasis by inactivating histone deacetylase 6 (HDAC6) during pulmonary fibrosis. Moreover, manipulation of primary cilia is an effective means to modulate the EMT program. Collectively, these results identify a pivotal role for the CYLD/HDAC6 signaling in regulating the reciprocal interplay between the EMT program and ciliary homeostasis during pulmonary fibrosis.

Indexed as

CiliaDeubiquitinating Enzyme CYLDEpithelial-Mesenchymal TransitionHistone Deacetylase 6HomeostasisPulmonary FibrosisSignal TransductionAnimalsBleomycinHumansMaleMiceMice, Inbred C57BLTransforming Growth Factor betaBleomycinCYLD protein, mouseDeubiquitinating Enzyme CYLDHdac6 protein, mouseHistone Deacetylase 6Transforming Growth Factor beta

Identifiers

PMID39122680
PMCPMC11316090

What OpenQuestion holds

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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.