ArticleRespiratory research2023
Role of mitochondrial fusion proteins MFN2 and OPA1 on lung cellular senescence in chronic obstructive pulmonary disease.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
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- Polymerized Z-α-1 antitrypsin leads to lung injury in a murine model of emphysema.JCI insight · 2026Article
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- Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.Biomolecules & therapeutics · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Mitochondria-endoplasmic reticulum contact sites in hepatocytic senescence.Cellular & molecular biology letters · 2026Review
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Mitochondrial Mechanisms of Resistance Exercise in COPD-Related Skeletal Muscle Dysfunction: A Narrative Review.International journal of chronic obstructive pulmonary disease · 2026Review
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Wnt signaling pathway in lung aging and aging-related chronic lung diseases.Biogerontology · 2025Review
- IFN-Mediated Bronchial Epithelium Cellular Senescence in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Double-edged mitophagy: balancing inflammation and resolution in lung disease.Clinical science (London, England : 1979) · 2025Review
- Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Senescence at the Crossroads of Lung Development and Injury.American journal of respiratory cell and molecular biology · 2025Article
- Identification and verification of mitochondria-related genes biomarkers associated with immune infiltration for COPD using WGCNA and machine learning algorithms.Scientific reports · 2025Article
- NLRP3 inflammasome-mediated disruption of mitochondrial homeostasis in alveolar macrophages contributes to ozone-induced acute lung inflammatory injury.Acta biochimica et biophysica Sinica · 2025Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundMitochondrial dysfunction and lung cellular senescence are significant features involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) stands as the primary contributing factor to COPD. This study examined mitochondrial dynamics, mitophagy and lung cellular senescence in COPD patients and investigated the effects of modulation of mitochondrial fusion [mitofusin2 (MFN2) and Optic atrophy 1 (OPA1)] on CS extract (CSE)-induced lung cellular senescence.
methodsSenescence-associated secretory phenotype (SASP) component mRNAs (IL-1β, IL-6, CXCL1 and CXCL8), mitochondrial morphology, mitophagy and mitochondria-related proteins (including phosphorylated-DRP1(p-DRP1), DRP1, MFF, MNF2, OPA1, PINK1, PARK2, SQSTM1/p62 and LC3b) and senescence-related proteins (including P16, H2A.X and Klotho) were measured in lung tissues or primary alveolar type II (ATII) cells of non-smokers, smokers and COPD patients. Alveolar epithelial (A549) cells were exposed to CSE with either pharmacologic inducer (leflunomide and BGP15) or genetic induction of MFN2 and OPA1 respectively.
resultsThere were increases in mitochondrial number, and decreases in mitochondrial size and activity in lung tissues from COPD patients. SASP-related mRNAs, DRP1 phosphorylation, DRP1, MFF, PARK2, SQSTM1/p62, LC3B II/LC3B I, P16 and H2A.X protein levels were increased, while MFN2, OPA1, PINK1 and Klotho protein levels were decreased in lung tissues from COPD patients. Some similar results were identified in primary ATII cells of COPD patients. CSE induced increases in oxidative stress, SASP-related mRNAs, mitochondrial damage and dysfunction, mitophagy and cellular senescence in A549 cells, which were ameliorated by both pharmacological inducers and genetic overexpression of MFN2 and OPA1.
conclusionsImpaired mitochondrial fusion, enhanced mitophagy and lung cellular senescence are observed in the lung of COPD patients. Up-regulation of MFN2 and OPA1 attenuates oxidative stress, mitophagy and lung cellular senescence, offering potential innovative therapeutic targets for COPD therapy.
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