ArticleAmerican journal of respiratory cell and molecular biology2019
Alternative Oxidase Attenuates Cigarette Smoke-induced Lung Dysfunction and Tissue Damage.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- An ancient oxidase lost in vertebrates promotes extreme stress tolerance in an emerging cnidarian model for ecology, evolution and biomedicine.The Journal of experimental biology · 2026Article
- Expression of yeast NADH dehydrogenase and ascidian alternative oxidase affects metabolism and free radical processes in Drosophila.BMC research notes · 2026Article
- The role of mitochondrial transfer in lung disease.Respiratory research · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Impairment of Muscle Function Causes Pupal Lethality in Flies Expressing the Mitochondrial Alternative Oxidase.Biomolecules · 2025Article
- Xenotopic synthetic biology: Prospective tools for delaying aging and age-related diseases.Science advances · 2025Review
- Comparative Assessment of Acute Pulmonary Effects Induced by Heat-Not-Burn Tobacco Aerosol Inhalation in a Murine Model.International journal of molecular sciences · 2025Article
- Elevated Urotensin-II and TGF-β Levels in COPD: Biomarkers of Fibrosis and Airway Remodeling in Smokers.Medicina (Kaunas, Lithuania) · 2024Article
- Alternative oxidase blunts pseudohypoxia and photoreceptor degeneration due to RPE mitochondrial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- GLUT3-mediated cigarette smoke-induced epithelial-mesenchymal transition in chronic obstructive pulmonary disease through the NF-kB/ZEB1 pathway.Respiratory research · 2024Article
- From Beach to the Bedside: Harnessing Mitochondrial Function in Human Diseases Using New Marine-Derived Strategies.International journal of molecular sciences · 2024Review
- Effective-Component Compatibility of Bufei Yishen Formula III Suppresses Mitochondrial Oxidative Damage in COPD: Via Pkm2/Nrf2 Pathway.International journal of chronic obstructive pulmonary disease · 2024Article
- Article
- Noncoupled Mitochondrial Respiration as Therapeutic Approach for the Treatment of Metabolic Diseases: Focus on Transgenic Animal Models.International journal of molecular sciences · 2023Review
- Alternative oxidase causes cell type- and tissue-specific responses in mutator mice.Life science alliance · 2023Article
- A Macrophage-Related Gene Signature for Identifying COPD Based on Bioinformatics and ex vivo Experiments.Journal of inflammation research · 2023Article
- Alternative oxidase encoded by sequence-optimized and chemically-modified RNA transfected into mammalian cells is catalytically active.Gene therapy · 2022Article
- Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension.Journal of clinical medicine · 2022Review
- Targeting the alternative oxidase (AOX) for human health and food security, a pharmaceutical and agrochemical target or a rescue mechanism?The Biochemical journal · 2022Review
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke (CS) exposure is the predominant risk factor for the development of chronic obstructive pulmonary disease (COPD) and the third leading cause of death worldwide. We aimed to elucidate whether mitochondrial respiratory inhibition and oxidative stress are triggers in its etiology. In different models of CS exposure, we investigated the effect on lung remodeling and cell signaling of restoring mitochondrial respiratory electron flow using alternative oxidase (AOX), which bypasses the cytochrome segment of the respiratory chain. AOX attenuated CS-induced lung tissue destruction and loss of function in mice exposed chronically to CS for 9 months. It preserved the cell viability of isolated mouse embryonic fibroblasts treated with CS condensate, limited the induction of apoptosis, and decreased the production of reactive oxygen species (ROS). In contrast, the early-phase inflammatory response induced by acute CS exposure of mouse lung, i.e., infiltration by macrophages and neutrophils and adverse signaling, was unaffected. The use of AOX allowed us to obtain novel pathomechanistic insights into CS-induced cell damage, mitochondrial ROS production, and lung remodeling. Our findings implicate mitochondrial respiratory inhibition as a key pathogenic mechanism of CS toxicity in the lung. We propose AOX as a novel tool to study CS-related lung remodeling and potentially to counteract CS-induced ROS production and cell damage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.