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Updated: May 1, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis
Jingrui Ren1, Ruijie Wan2, Shuai Zhou3
1Department of Geriatrics, People's Hospital of Zhengzhou University, No. 100 Science Avenue, High-Tech Zone, Zhengzhou, Henan Province, China.
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.
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