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Background <p>Idiopathic pulmonary fibrosis (IPF) is a progressive lung disorder with few effective treatments. This study examines how Krüppel-like factor 14 (KLF14) influences fatty acid oxidation (FAO) and fibroblast senescence in IPF.</p> Methods <p>A rat model of IPF was induced using bleomycin. Expression levels of KLF14, CPT1A, and related proteins were measured using qRT-PCR and Western blot. Lung tissue histology was examined, and cellular senescence was evaluated using SA-β-gal staining. The transcriptional regulation of CPT1A by KLF14 was confirmed through luciferase reporter assays and ChIP.</p> Results <p>KLF14 expression was significantly downregulated in the IPF model. Overexpression of KLF14 reduced collagen deposition, attenuated fibroblast senescence, and enhanced FAO by upregulating CPT1A. Mechanistically, KLF14 binds to the CPT1A promoter, promoting its transcription.</p> Conclusions <p>KLF14 enhances FAO through CPT1A activation, offering a novel therapeutic strategy for IPF.</p> Graphical Abstract <p>Schematic summary illustrating the mechanism by which KLF14 alleviates pulmonary fibrosis through restoration of FAO, and inhibition of fibroblast transdifferentiation and senescence.</p> <p></p>

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Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月30日

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  • Jingrui Ren,
  • Ruijie Wan,
  • Shuai Zhou,
  • Xinran Ma,
  • Chenxi Zhu,
  • Jinxin Ma,
  • Jianqiao Chen,
  • Limin Zhao,
  • Wenjuan Wu

摘要

Background

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disorder with few effective treatments. This study examines how Krüppel-like factor 14 (KLF14) influences fatty acid oxidation (FAO) and fibroblast senescence in IPF.

Methods

A rat model of IPF was induced using bleomycin. Expression levels of KLF14, CPT1A, and related proteins were measured using qRT-PCR and Western blot. Lung tissue histology was examined, and cellular senescence was evaluated using SA-β-gal staining. The transcriptional regulation of CPT1A by KLF14 was confirmed through luciferase reporter assays and ChIP.

Results

KLF14 expression was significantly downregulated in the IPF model. Overexpression of KLF14 reduced collagen deposition, attenuated fibroblast senescence, and enhanced FAO by upregulating CPT1A. Mechanistically, KLF14 binds to the CPT1A promoter, promoting its transcription.

Conclusions

KLF14 enhances FAO through CPT1A activation, offering a novel therapeutic strategy for IPF.

Graphical Abstract

Schematic summary illustrating the mechanism by which KLF14 alleviates pulmonary fibrosis through restoration of FAO, and inhibition of fibroblast transdifferentiation and senescence.