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Integrated multiomic analysis identifies TRIP13 as a mediator of alveolar epithelial type II cell dysfunction in idiopathic pulmonary fibrosis
Journal article   Peer reviewed

Integrated multiomic analysis identifies TRIP13 as a mediator of alveolar epithelial type II cell dysfunction in idiopathic pulmonary fibrosis

Laurence St. Pierre, Asres Berhan, Eun K. Sung, Juan R. Alvarez, Hongjun Wang, Yanbin Ji, Yixin Liu, Haoze Yu, Angela Meier, Kamyar Afshar, …
Biochimica et biophysica acta. Molecular basis of disease, Vol.1871(3), 167572
03/2025
DOI: 10.1016/j.bbadis.2024.167572
PMCID: PMC11951472
PMID: 39547519

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Abstract

Idiopathic pulmonary fibrosis (IPF) is a lethal progressive lung disease urgently needing new therapies. Current treatments only delay disease progression, leaving lung transplant as the sole remaining option. Recent studies support a model whereby IPF arises because alveolar epithelial type II (AT2) cells, which normally mediate distal lung regeneration, acquire airway and/or mesenchymal characteristics, preventing proper repair. Mechanisms driving this abnormal differentiation remain unclear. We performed integrated transcriptomic and epigenomic analysis of purified AT2 cells which revealed genome-wide alterations in IPF lungs. The most prominent epigenetic alteration was activation of an enhancer in thyroid receptor interactor 13 (TRIP13), although TRIP13 was not the most significantly transcriptionally upregulated gene. TRIP13 is broadly implicated in epithelial-mesenchymal plasticity. In cultured human AT2 cells and lung slices, small molecule TRIP13 inhibitor DCZ0415 prevented acquisition of the mesenchymal gene signature characteristic of IPF, suggesting TRIP13 inhibition as a potential therapeutic approach to fibrotic disease. [Display omitted] •Genome-wide transcriptomic and epigenomic alterations in IPF AT2 cells•TRIP13 expression elevated in IPF distal lung epithelium.•TRIP13 inhibition prevents epithelial-mesenchymal transition in human AT2 cells.•TRIP13 modulates STAT3 and WNT/β-catenin pathways in AT2 cells.•TRIP13 may be a novel therapeutic target in IPF.
ATAC-seq Epigenomic analysis Epithelial-mesenchymal plasticity Idiopathic pulmonary fibrosis (IPF) RNA-seq TRIP13

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