ArticleEBioMedicine2019
Mitochondrial dysfunction in human primary alveolar type II cells in emphysema.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 84 citations in OpenAlex.
- Fuelling repair: metabolic regulation of alveolar type 2 cell fate in lung regeneration and disease.Disease models & mechanisms · 2026Review
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- Smoker's Lungs: Quo Vadis? Exploring the Shared and Individual Smoking-Related Molecular Pathways of Emphysema, Carcinoma, and Fibrosis - An Illustrative Review.Thoracic cancer · 2026Review
- Adenine nucleotide translocase 2 (ANT2) deficiency reprograms ferroptosis in alveolar progenitor cells to promote emphysema.bioRxiv : the preprint server for biology · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Mitochondrial transplantation in lung diseases: From mechanisms to application prospects.Genes & diseases · 2026Review
- CerS6 orchestrates mitochondrial-immune crosstalk via BNIP3-dependent mitophagy suppression and mtDNA-STING/NLRP3 activation in acute lung injury.Cellular and molecular life sciences : CMLS · 2026Article
- Stiffness-dependent alveolar type II cell senescence in idiopathic pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- Epigenetic dysregulation of IRF9 drives excessive interferon signaling in COPD.EMBO molecular medicine · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026Article
- Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Involvement of mitochondrial unfolded protein response and activating transcription factor 4 in the mitochondrial damage pathway of BEAS-2B cells induced by cigarette smoke extracts.Journal of thoracic disease · 2025Article
- An integrated investigation of mitochondrial genes in COPD reveals the causal effect of NDUFS2 by regulating pulmonary macrophages.Biology direct · 2025Article
- LBH589 reduces oxidized mitochondrial DNA and suppresses NLRP3 inflammasome activation to relieve pulmonary inflammation.PloS one · 2025Article
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Extreme temperatures modulate gene expression in the airway epithelium of the lungs in mice and asthma patients.Frontiers in medicine · 2025Article
- The Effective Compound Combination of Bufei Yishen Formula III Improves the Mitochondrial Dysfunction via Inhibiting JNK/Sab Pathway in COPD Mice.Drug design, development and therapy · 2025Article
- Unlocking lung regeneration: insights into progenitor cell dynamics and metabolic control.Cell regeneration (London, England) · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCigarette smoke is the main risk factor of pulmonary emphysema development, which is characterized by alveolar wall destruction. Mitochondria are important for alveolar type II (ATII) cell metabolism due to ATP generation.
methodsWe isolated ATII cells from control non-smoker and smoker organ donors, and after lung transplant of patients with emphysema to determine mitochondrial function, dynamics and mitochondrial (mt) DNA damage.
findingsWe found high mitochondrial superoxide generation and mtDNA damage in ATII cells in emphysema. This correlated with decreased mtDNA amount. We also detected high TOP1-cc and low TDP1 levels in mitochondria in ATII cells in emphysema. This contributed to the decreased resolution of TOP1-cc leading to accumulation of mtDNA damage and mitochondrial dysfunction. Moreover, we used lung tissue obtained from areas with mild and severe emphysema from the same patients. We found a correlation between the impaired fusion and fission as indicated by low MFN1, OPA1, FIS1, and p-DRP1 levels and this disease severity. We detected lower TDP1 expression in severe compared to mild emphysema.
interpretationWe found high DNA damage and impairment of DNA damage repair in mitochondria in ATII cells isolated from emphysema patients, which contribute to abnormal mitochondrial dynamics. Our findings provide molecular mechanisms of mitochondrial dysfunction in this disease. FUND: This work was supported by National Institutes of Health (NIH) grant R01 HL118171 (B.K.) and the Catalyst Award from the American Lung Association (K.B.).
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Registered trials
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