ArticleClinical science (London, England : 1979)2023
Cigarette smoke induces mitochondrial DNA damage and activates cGAS-STING pathway: application to a biomarker for atherosclerosis.
Article in Clinical science (London, England : 1979), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Prodh2-Mediated Mitochondrial Stress Drives TNF-α-Induced Myoblast Dysfunction and Sarcopenia in COPD.Aging cell · 2026Article
- Endothelial Filamin C Alleviates Atherosclerosis via PINK1/Parkin-Dependent Mitophagy and mtDNA-cGAS-STING Inflammation Suppression.Journal of cardiovascular development and disease · 2026Article
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Cigarette Smoke Extract Alters the Inflammatory Secretome of Osteoarthritis-Affected Synovium Increasing Joint Tissue Oxidative Stress in an Indirect Co-Culture Model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- cGAS knockout inhibited endotoxin-induced uveitis in mice.Genes & diseases · 2026Article
- Systematic Identification and Functional Validation of CASP10 as a DNA-Damage-Responsive Driver of Endothelial Pyroptosis in Atherosclerosis.Journal of cellular and molecular medicine · 2026Article
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- Prevalence and risk factors of cognitive impairment in patients with coronary heart disease: a systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2026Review
- Research progress on the mechanisms of cGAS-STING signaling in immune cell infiltration associated with vascular remodeling.Journal of translational medicine · 2025Review
- Metabolic Remodeling and Mitochondrial Stress in Atrial Fibrillation: Mechanisms and Translational Targets.Reviews in cardiovascular medicine · 2025Review
- Self-DNA by Activating the CGAS-STING1 Pathway Contributes to the Pathogenesis of Atherosclerosis.Current atherosclerosis reports · 2025Review
- Sex-specific mitochondrial DNA changes in neuron-derived extracellular vesicles of African American adults: impact of HIV infection and smoking.Journal of neurovirology · 2025Article
- Clinical changes of cardiac function from high altitude returning to plain.Scientific reports · 2025Article
- Emerging role of the cGAS-STING pathway in cardiovascular diseases: biologic function, mechanisms and targeted therapy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Bidirectional regulation of the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon gene pathway and its impact on hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- Mitochondrial DNA in atherosclerosis research progress: a mini review.Frontiers in immunology · 2025Review
- Uncovering the Role of Anmeidan against Atherosclerosis from Integrated Network Pharmacology and Pharmacological Experiments.Combinatorial chemistry & high throughput screening · 2025Article
- The activation of cGAS-STING pathway causes abnormal uterine receptivity in aged mice.Aging cell · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking is a major risk factor for atherosclerosis. We previously reported that DNA damage was accumulated in atherosclerotic plaque, and was increased in human mononuclear cells by smoking. As vascular endothelial cells are known to modulate inflammation, we investigated the mechanism by which smoking activates innate immunity in endothelial cells focusing on DNA damage. Furthermore, we sought to characterize the plasma level of cell-free DNA (cfDNA), a result of mitochondrial and/or genomic DNA damage, as a biomarker for atherosclerosis. Cigarette smoke extract (CSE) increased DNA damage in the nucleus and mitochondria in human endothelial cells. Mitochondrial damage induced minority mitochondrial outer membrane permeabilization, which was insufficient for cell death but instead led to nuclear DNA damage. DNA fragments, derived from the nucleus and mitochondria, were accumulated in the cytosol, and caused a persistent increase in IL-6 mRNA expression via the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. cfDNA, quantified with quantitative PCR in culture medium was increased by CSE. Consistent with in vitro results, plasma mitochondrial cfDNA (mt-cfDNA) and nuclear cfDNA (n-cfDNA) were increased in young healthy smokers compared with age-matched nonsmokers. Additionally, both mt-cfDNA and n-cfDNA were significantly increased in patients with atherosclerosis compared with the normal controls. Our multivariate analysis revealed that only mt-cfDNA predicted the risk of atherosclerosis. In conclusion, accumulated cytosolic DNA caused by cigarette smoke and the resultant activation of the cGAS-STING pathway may be a mechanism of atherosclerosis development. The plasma level of mt-cfDNA, possibly as a result of DNA damage, may be a useful biomarker for atherosclerosis.
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Registered trials
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.