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Epithelial QKI Protects Against Emphysema by Maintaining Mitochondrial Integrity
Preprint   Open access

Epithelial QKI Protects Against Emphysema by Maintaining Mitochondrial Integrity

Kiyoshi Uemasu, Kazuya Tanimura, Atsushi Miyamoto, Koichi Hasegawa, Zachary Lane, Reika Nyunoya, Haruka Uemasu, Brett A Kaufman, Corrine R Kliment, Divay Chandra, …
bioRxiv
Cold Spring Harbor Laboratory
07/10/2026
DOI: 10.64898/2026.07.09.737340
PMID: 42465480
url
https://doi.org/10.64898/2026.07.09.737340View
Preprint (Author's original) This preprint has not been evaluated by subject experts through peer review. Preprints may undergo extensive changes and/or become peer-reviewed journal articles. Open Access

Abstract

Single-cell transcriptomic profiling of chronic obstructive pulmonary disease (COPD) lungs identified QKI, an RNA-binding protein, as a candidate emphysema-associated gene, but its epithelial role in COPD pathobiology remains unclear. We show that QKI expression is reduced in human COPD lungs and that alveolar type 2 epithelial (AT2) cell QKI protein levels correlate strongly with spirometric indices and diffusing capacity (DL ). Lung epithelium-specific QKI knockout mice (QKI ) developed spontaneous airspace enlargement with emphysema-like mechanics, and QKI-deficient AT2 cells showed impaired spheroid colony formation and increased apoptosis. Integrated transcriptomic and proteomic analyses of primary AT2 cells revealed a selective reduction in functional mitochondrial (respiratory-chain and metabolic) protein abundance despite relatively preserved transcript levels, consistent with mitochondrial transcriptome-proteome discordance. QKI loss increased mtDNA abundance and TOMM20 staining but decreased ATP5A, indicating accumulation of structurally increased but functionally dysfunctional mitochondria. In human epithelial cells, CRISPR-mediated QKI deficiency reduced oxidative respiration, increased glycolytic reliance, elevated mitochondrial ROS and membrane potential, and increased apoptosis; these phenotypes were partially rescued by QKI re-expression. These findings identify epithelial QKI as a regulator of mitochondrial integrity and stress tolerance in COPD.

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