A newly issued publisher correction in Experimental & Molecular Medicine has drawn attention to a research model designed to examine how human lung tissue adapts to prolonged exposure to cigarette smoke. The corrected article, titled “A chronic whole cigarette smoke extract model reveals redox–mitochondrial adaptation in human lung epithelial and organoid models,” is authored by JE Lee, D. Lee, J. Lee and colleagues, and is identified by the 2026 DOI 10.1038/s12276-026-01829-6. While the notice is formally a correction to the published record, the study’s subject highlights a central challenge in respiratory biology: understanding how cells respond when smoke exposure becomes persistent rather than brief.
Most laboratory studies of cigarette smoke toxicity rely on short-term exposure experiments. These can reveal immediate cellular damage, including oxidative stress, inflammatory signaling and mitochondrial dysfunction, but they may not fully reproduce the biological conditions created by repeated exposure over months or years. A chronic whole cigarette smoke extract model attempts to bridge that gap by exposing lung-derived cells to a complex mixture that more closely reflects the chemical diversity of cigarette smoke. Such mixtures contain reactive oxygen species, aldehydes, polycyclic aromatic hydrocarbons, nicotine and numerous other compounds capable of affecting DNA, proteins, membranes and intracellular energy systems.
The research described by the article focuses on human lung epithelial cells and organoids. Lung epithelial cells form the protective interface between inhaled air and deeper tissues, while organoids are three-dimensional laboratory-grown structures that can reproduce selected features of native tissue architecture. Unlike flat cell cultures, organoids allow researchers to study how cells organize, communicate and respond within a more tissue-like environment. This distinction is important because smoke-related injury is not determined solely by what happens inside an isolated cell; it also depends on cell-to-cell interactions, structural organization and the ability of tissue to repair itself.
A central concept in the study is redox biology, which examines the balance between oxidizing and reducing chemical reactions inside cells. Cigarette smoke can overwhelm antioxidant defenses by increasing the production of reactive oxygen species and reactive nitrogen species. These chemically active molecules can modify proteins, damage lipids and interfere with genetic material. However, oxidative molecules are not exclusively destructive. At controlled levels, they also act as signals that activate protective pathways. A chronic exposure model can therefore reveal whether lung cells remain in a state of ongoing injury or develop adaptive responses that help them survive continued chemical stress.
Mitochondria are particularly important in this context because they generate most of the cell’s usable energy while also contributing to redox regulation and programmed cell death. Smoke-derived compounds can impair the mitochondrial electron transport chain, reduce energy production and increase the leakage of electrons that form reactive oxygen species. Cells may respond by changing mitochondrial metabolism, adjusting antioxidant systems, altering the removal of damaged mitochondria or reorganizing how they generate energy. These adaptations can preserve short-term survival, but they may also carry long-term costs if they allow damaged cells to persist or reduce the tissue’s capacity for normal repair.
The phrase “redox–mitochondrial adaptation” points to an interconnected response rather than a single molecular event. A change in cellular redox balance can influence mitochondrial activity, while mitochondrial stress can further reshape the redox environment. This feedback may activate transcription factors that regulate antioxidant enzymes, metabolic pathways and stress-response genes. In epithelial tissue, such changes could affect barrier function, differentiation and regeneration. Organoids provide a way to investigate these effects over time, allowing researchers to compare acute damage with the more complex state that develops after repeated exposure.
The importance of the model extends beyond cigarette research. Chronic inhalation-related diseases often arise from the interaction of repeated environmental stress, genetic susceptibility and imperfect tissue repair. A system that combines human lung cells, three-dimensional organization and prolonged exposure may help scientists test why some cells recover while others enter persistent dysfunction. It could also support the evaluation of potential therapies aimed at restoring mitochondrial performance, strengthening antioxidant defenses or preventing maladaptive cellular states. Such applications remain experimental, and laboratory findings cannot by themselves predict how an individual smoker will respond.
The publication now carries a publisher correction, meaning that the formal scientific record has been updated by the journal. The citation identifies the work as a correction associated with the study, but the bibliographic information provided does not specify the exact text, figure, author or data element that was amended. Readers should therefore consult the corrected version at the journal’s website when precise interpretation is required. Even so, the study’s broader message remains scientifically significant: understanding smoke-related lung disease requires models that capture not only immediate toxicity, but also the biological adaptations that emerge when exposure continues over time.
Subject of Research: Chronic cigarette smoke exposure, redox biology, mitochondrial adaptation, human lung epithelial cells and lung organoid models
Article Title: Publisher Correction: A chronic whole cigarette smoke extract model reveals redox–mitochondrial adaptation in human lung epithelial and organoid models
Article References: Lee, JE., Lee, D., Lee, J. et al. Publisher Correction: A chronic whole cigarette smoke extract model reveals redox–mitochondrial adaptation in human lung epithelial and organoid models. Experimental & Molecular Medicine (2026). https://doi.org/10.1038/s12276-026-01829-6
Image Credits: AI Generated
DOI: 10.1038/s12276-026-01829-6
Keywords: cigarette smoke extract, chronic exposure, lung epithelial cells, organoids, redox adaptation, mitochondrial function, oxidative stress, respiratory biology
Tags: cellular response to prolonged smoke exposurechronic lung tissue adaptationcigarette smoke exposure modelcomplex chemical composition of cigarette smokeexperimental models of cigarette smoke toxicityhuman lung epithelial cellslong-term cigarette smoke effectslung organoid modelsmitochondrial dysfunction in lungsoxidative stress in respiratory cellsredox-mitochondrial responserespiratory biology and smoke toxicity
