ArticleClinical epigenetics2025
HMGA1 drives EMT in obliterative bronchiolitis through epigenetic regulation of chromatin accessibility in pulmonary epithelial cells.
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Lung transplantation in 2025: a narrative review of progress, challenges, and the road ahead.Journal of thoracic disease · 2026Review
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundPost-transplant obliterative bronchiolitis (OB) is a major cause of lung graft dysfunction and failure, with the epithelial-mesenchymal transition (EMT) process playing a pivotal role in driving extracellular matrix (ECM) deposition and fibrosis.
methodsA mouse heterotopic tracheal allograft model was established to replicate the clinical manifestations of post-transplant OB. Histopathological alterations of tracheal grafts were assessed using Hematoxylin and Eosin (HE) staining. Gene expression was quantified through enzyme-linked immunosorbent assay (ELISA), immunofluorescence (IF), immunohistochemistry (IHC), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot assays. Differentially expressed genes (DEGs) in heterotopic tracheal grafts were identified by RNA sequencing (RNA-Seq). Chromatin accessibility was evaluated using assay for transposase-accessible chromatin with sequencing (ATAC-Seq).
resultsHistological analysis revealed progressive luminal occlusion (7-14 days), with significant inflammatory infiltration at day 7 and ECM deposition at day 14. Elevated IL-1β/IL-6 levels and reduced IL-10 confirmed immune activation. High mobility group at-hook 1 (HMGA1) was upregulated in allografts and mediated TGF-β1-driven EMT in vitro. Integration of ATAC-seq and RT-qPCR in pulmonary epithelial cells demonstrated that HMGA1 orchestrates extensive chromatin remodeling during OB pathogenesis. HMGA1 directly enhanced chromatin accessibility at EMT-promoting loci, including specificity protein 1 (SP1), dedicator of cytokinesis 4 (DOCK4), serum response factor (SRF), and anillin (ANLN). Epigenetic reprogramming of these regulatory regions induced TGF-β1-mediated EMT.
conclusionsHMGA1 promotes EMT in OB by facilitating chromatin accessibility at EMT-associated loci, highlighting its potential as a therapeutic target for post-transplant intervention.
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