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Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
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Published on: May 9, 2025

Ceramide-Driven Mechanisms in Pulmonary Fibrosis.

Zifan Li1, Yaqian Li2, Na Mao1

  • 1School of Public Health, North China University of Science and Technology, Tangshan 063000, China.

Metabolites
|June 25, 2026
PubMed
Summary

This review highlights how ceramide accumulation drives pulmonary fibrosis. Targeting ceramide metabolism offers new therapeutic strategies for idiopathic pulmonary fibrosis (IPF) and other fibrotic lung diseases.

Keywords:
acid sphingomyelinaseceramidefibroblast activationpulmonary fibrosissphingolipid

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Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

Area of Science:

  • Pulmonary medicine
  • Cell biology
  • Biochemistry

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options.
  • Dysregulated sphingolipid metabolism, particularly ceramide accumulation, is increasingly recognized as a key factor in fibrosis.
  • Ceramide influences critical cellular processes like apoptosis, inflammation, and fibroblast activation, contributing to lung damage.

Purpose of the Study:

  • To systematically review ceramide's role in pulmonary fibrosis.
  • To explore ceramide's biosynthetic and metabolic pathways, including chain length-specific functions.
  • To discuss therapeutic strategies targeting ceramide metabolism for fibrotic lung diseases.

Main Methods:

  • This study is a narrative review.
  • It systematically summarizes existing literature on ceramide metabolism and its role in pulmonary fibrosis.
  • It analyzes the mechanistic functions of ceramide in lung disease pathogenesis.

Main Results:

  • Ceramide accumulation is a significant driver of fibrotic pathogenesis in the lungs.
  • Specific ceramide chain lengths and the ceramide to S1P rheostat are crucial in regulating fibrotic processes.
  • Ceramide contributes to alveolar epithelial cell apoptosis, inflammation, and vascular barrier dysfunction.

Conclusions:

  • Targeting ceramide metabolism presents a promising therapeutic avenue for pulmonary fibrosis.
  • Inhibitors of acid sphingomyelinase (ASMase) and serine palmitoyltransferase (SPT) are potential treatments.
  • Further research is needed for clinical translation of these ceramide-targeting strategies.