FABP4‐mediated lipid droplet accumulation drives epithelial–mesenchymal transition and aggravates alveolar epithelial barrier disruption

LIRI induces autocrine FABP4 signaling in alveolar epithelial cells. FABP4 promotes lipid droplets accumulation by inhibiting lipophagy through p38 MAPKULK1 signaling. FABP4-driven lipid metabolic reprogramming triggers EMT and disrupts alveolar epithelial barrier integrity. Targeting FABP4 or lipid droplets accumulation may offer therapeutic potential for CPB-associated ARDS.

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Publication Details

Journal
Clinical and Translational Medicine
Published
2025-12-26
DOI
https://doi.org/10.1002/ctm2.70563
Primary Topic
Peroxisome Proliferator-Activated Receptors
Type
article
Field-Weighted Citation Impact
0.00
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article

FABP4‐mediated lipid droplet accumulation drives epithelial–mesenchymal transition and aggravates alveolar epithelial barrier disruption

Min Wu, Mingyu Chu, Linjie Si, X. T. Li et al.
Clinical and Translational Medicine
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FABP4‐mediated lipid droplet accumulation drives epithelial–mesenchymal transition and aggravates alveolar epithelial barrier disruption

Min Wu, Mingyu Chu, Linjie Si, X. T. Li, Jialin Zhang, Ye Wang, Xiaoning Lu, Peng Lü, Zihao Shen, Z. Liu, Yuanpu Qi, Chen Feng
article en

Abstract

LIRI induces autocrine FABP4 signaling in alveolar epithelial cells. FABP4 promotes lipid droplets accumulation by inhibiting lipophagy through p38 MAPKULK1 signaling. FABP4-driven lipid metabolic reprogramming triggers EMT and disrupts alveolar epithelial barrier integrity. Targeting FABP4 or lipid droplets accumulation may offer therapeutic potential for CPB-associated ARDS.

Clinical and Translational MedicineVol. 16(1)
Nanjing Medical University (CN)
Good health and well-being
Openalex Percentile: Top 36%
Peroxisome Proliferator-Activated Receptors
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