ArticleRedox biology2021
Role of inner mitochondrial protein OPA1 in mitochondrial dysfunction by tobacco smoking and in the pathogenesis of COPD.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Regulation of mitochondrial fission by Drp1 in cardiomyopathy: possible mechanisms linking cellular processes to cell death.Molecular biology reports · 2026Review
- Heavy Metal Transfer from Cigarette Smoke to Lung Tissue: Inducing on Pulmonary Function and Bronchoalveolar Microbiome Dysregulation in Rats.Biological trace element research · 2026Article
- Oxidative stress-associated genes TPPP3 and VEGFA in COPD revealed by bulk and single-cell sequencing analysis.Scientific reports · 2026Article
- Decoding serum C-reactive protein-associated molecular patterns in aging and secondhand smoke exposure chronic obstructive pulmonary disease male patients: evidence from cross-sectional, multi-omic and clinical studies.Frontiers in medicine · 2026Article
- Health effects of black and blond tobacco: a comparative analysis on smoking-related diseases with emphasis on bronchitis and COPD.Frontiers in public health · 2026Article
- HtrA2/Omi: potential therapeutic targets for neurodegenerative diseases.Frontiers in pharmacology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- 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
- Effects of in utero tobacco exposure, age of smoking initiation, and environmental pollution on the risk of chronic obstructive pulmonary disease in adulthood: a large scale prospective cohort study.BMC pulmonary medicine · 2025Article
- Reactive Oxygen Species-Mediated TRPM2 Activation Facilitates Phagocytosis of Macrophages to Reverse Profibrotic Phenotype.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Article
- OPA1 Enhances Microglial Amyloid-β Clearance and Alleviates Cognitive Impairments in an Alzheimer's Disease Model.Aging and disease · 2025Article
- An integrated investigation of mitochondrial genes in COPD reveals the causal effect of NDUFS2 by regulating pulmonary macrophages.Biology direct · 2025Article
- Bioinformatics identification of mitochondria and macrophage polarization-related genes in COPD and their potential mechanisms.Frontiers in immunology · 2025Article
- Modulating mitochondria with natural extract compounds: from bench to clinical therapeutic opportunities for COPD.Frontiers in pharmacology · 2025Review
- Identification of Cuproptosis-Related Genes and Their Potential Role in COPD Pathogenesis: A Bioinformatics Analysis.International journal of chronic obstructive pulmonary disease · 2025Article
- Mitochondrial transfer/transplantation in lung injury: mechanism, therapeutic potential, and clinical application.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic lung diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are linked to several mitochondrial alterations. Cigarette smoke (CS) alters the structure and function of mitochondria. OPA1 is the main inner mitochondrial GTPase responsible for the fusion events. OPA1 undergoes proteolytic cleavage from long to short forms during acute stress and mitophagy. However, the exact role of OPA1 isoforms and related proteins during CS-induced mitophagy and COPD is not clear.
methodsLung tissues from non-smokers, smokers, COPD and IPF were used to determine the relative expression of OPA1 and related proteins. Additionally, we used mouse lungs from chronic (6 months) CS exposure to evaluate the status of OPA1. Primary lung fibroblasts from normal and COPD patients and naked mole rat (NMR) lung fibroblasts, human fetal lung fibroblast (HFL1), mouse embryonic fibroblast from wild type (WT), OPA1
findingsShort OPA1 isoforms were predominantly detected and significantly increased in COPD subjects. Acute CSE treatment in various cell lines except NMR was found to increase the conversion of long to short OPA1 isoforms. CSE treatment significantly increased mitochondrial stress-related protein SLP2 in all the cells used. OPA1 interacting partners like prohibitins (PHB1 and 2) were also altered depending on the CS exposure. Finally, BGP-15 and leflunomide treatment were able to preserve the long OPA1 isoform in cells treated with CSE. INTERPRETATION/
conclusionThe long OPA1 isoform along with SLP2 and prohibitins play a crucial role in CS-induced lung damage, causing mitophagy/mitochondrial dysfunction in COPD, which may be used as a novel therapeutic target in COPD.
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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 Socratic graph.