Evidence map›Paper›PMID 40750768›Full record

ArticleScientific reports2025

High-selective HDAC6 inhibitor alleviates bone marrow fibrosis through inhibiting collagen formation and extracellular matrix deposition.

Chiao-Hsu Ke, Mao-En Huang, Hsin-Yi Wu, Chao-Wu Yu, Shuei-Liong Lin, Shau-Ping Lin, Shu-Han Yu, Chih-Hung Huang, Chen-Si Lin

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Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Chiao-Hsu KeDepartment of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei, 10617, Taiwan, ROC.
Mao-En HuangDepartment of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei, 10617, Taiwan, ROC.
Hsin-Yi WuInstrumentation Center, National Taiwan University, Taipei, 10617, Taiwan.
Chao-Wu YuSchool of Pharmacy, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shuei-Liong LinGraduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei, 100, Taiwan.
Shau-Ping LinAgricultural Biotechnology Research Center, Academia Sinica, Taipei, 115, Taiwan.
Shu-Han YuInstitute of Biotechnology, National Taiwan University, Taipei, 106, Taiwan.
Chih-Hung HuangDepartment of Chemical Engineering and Biotechnology, Institute of Chemical Engineering, National Taipei University of Technology, Taipei, 10608, Taiwan.
Chen-Si LinDepartment of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd., Taipei, 10617, Taiwan, ROC. cslin100@ntu.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow fibrosis (BMF) impairs normal hematopoietic functions in patients. The overactivation of the TGF-β signaling pathway is regarded as one of the offenders causing disease progression. Thus, factors capable of regulating TGF-β secretion hold great potential in reversing fibrotic diseases. One such factor is histone deacetylase inhibitors (HDACis), which can modulate the expression of TGF-β. Our previous study successfully synthesized a selective HDAC6 inhibitor, J22352, for pulmonary fibrosis; however, the treatment efficacies on BMF remain unclear. Therefore, in this study, we treated bone marrow-derived myofibroblasts with J22352. The results showed that J22352 significantly reduced cell viability, induced apoptosis, and inhibited extracellular matrix (ECM) accumulation. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis was employed to disclose potential mechanisms, identifying 334 differentially expressed proteins (DEPs). The DEPs were involved in cell apoptosis, programmed cell death, ECM deposition, and collagen formation. These results suggest that J22352 efficiently alleviated BMF by inducing cell apoptosis and inhibiting ECM deposition. This study introduces a novel selective HDAC6 inhibitor as a potential option for slowing down the progression of BMF. We aim to provide a promising selective HDACi for clinical medicine through a detailed analysis of its mechanisms and efficacy, offering new prospects in the field.

Indexed as

Bone MarrowCollagenExtracellular MatrixHistone Deacetylase 6Histone Deacetylase InhibitorsAnimalsApoptosisCell SurvivalFibrosisHumansMiceMyofibroblastsSignal TransductionTransforming Growth Factor betaCollagenHdac6 protein, mouseHistone Deacetylase 6Histone Deacetylase InhibitorsTransforming Growth Factor betaBone marrow fibrosisHistone deacetylase inhibitorOrgan fibrosisTransforming growth factor-β (TGF-β)

Identifiers

PMID40750768
PMCPMC12317122

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