LncRNA HOTAIR contributes to cigarette smoke-induced pro-inflammatory responses in human airway epithelial cells

American Journal of Physiology-Lung Cellular and Molecular Physiology 2026 Open access

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Authors: Xinzi Zheng, Priscila Pineda-Villegas, Martijn C. Nawijn, Irene H. Heijink
DOI: 10.1152/ajplung.00126.2025
Cited by: 1
References: 44

Abstract

COPD-derived AECs exhibit higher susceptibility to CSE-induced HOTAIR upregulation. CSE induces distinct histone modification patterns (H3K4me3) specifically in COPD-derived AECs. HOTAIR is essential for mediating CSE-induced proinflammatory responses in AECs.

Fields of Study & Subjects

Cancer-related molecular mechanisms research Epigenetics and DNA Methylation Genomics and Chromatin Dynamics

Publication details

Journal / source
American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher
American Physiological Society
Volume
330
Issue
4
Pages
L446–L456
Publication date
4 March 2026
Language
EN