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Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
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Introduction to Fibroblasts01:09

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...

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Related Experiment Video

Updated: May 17, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

NAT10-dependent ac4C mRNA modification programs fibroblast pathogenicity in systemic sclerosis.

Weibo Tang1, Ye Xu2, Wenya Liu3

  • 1State Key Laboratory of Macromolecular Drugs and Large-scale Manufacturing, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou 325000, China; Translational Medicine Laboratory, Jilin Medical University, Jilin 132013, China.

Pharmacological Research
|May 15, 2026
PubMed
Summary
This summary is machine-generated.

N-acetyltransferase 10 (NAT10) RNA modification drives fibroblast activation in systemic sclerosis (SSc). Targeting this NAT10-ac4C pathway may offer new therapies for fibrotic diseases.

Keywords:
EpigeneticsHuman dermal fibroblastsNAT10Systemic sclerosismRNA ac4C modification

Related Experiment Videos

Last Updated: May 17, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Area of Science:

  • Epitranscriptomics
  • Fibrotic Diseases
  • Molecular Mechanisms

Background:

  • Systemic sclerosis (SSc) involves progressive fibrosis due to activated dermal fibroblasts.
  • Epigenetic and epitranscriptomic regulators of fibroblast pathogenicity in SSc are not fully understood.

Purpose of the Study:

  • Investigate the role of N-acetyltransferase 10 (NAT10) and its N4-acetylcytidine (ac4C) RNA modification in fibroblast activation and SSc fibrosis.
  • Identify downstream targets and mechanisms of NAT10 in fibrotic remodeling.

Main Methods:

  • Integrative analysis of single-cell transcriptomics, human SSc skin samples, in vitro assays, and in vivo models.
  • Fibroblast-specific knockout mice were used to study NAT10 function.
  • Multi-omics analyses identified NAT10 targets and ac4C modification sites.

Main Results:

  • NAT10 is upregulated in pathogenic fibroblasts and promotes fibrotic progression in SSc models.
  • NAT10 inhibition reduced fibroblast proliferation and extracellular matrix deposition.
  • ac4C modification on COL11A1 and ZNF621 transcripts increased their stability and expression, promoting fibrosis.

Conclusions:

  • Defines a novel epitranscriptomic mechanism involving NAT10-mediated ac4C modification in SSc fibroblast activation.
  • Suggests the NAT10-ac4C axis as a potential therapeutic target for SSc and other fibrotic diseases.