ArticleInternational journal of biological sciences2019
The Antioxidant MitoQ Protects Against CSE-Induced Endothelial Barrier Injury and Inflammation by Inhibiting ROS and Autophagy in Human Umbilical Vein Endothelial Cells.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 81 citations in OpenAlex.
- Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.GeroScience · 2026Review
- Influence of heat-non-burn tobacco aerosol on the microbiome of biofilm from human whole saliva bacteria in vitro.Clinical oral investigations · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- Endothelial mitochondrial homeostasis in the development and progression of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Ginsenoside Rg1 Alleviates Hydrogen Peroxide-Induced Autophagy and Apoptosis in Ovarian Granulosa Cells.Cell biochemistry and biophysics · 2025Article
- NLRP3-Mediated PANoptosis and Associated Interventions in Endothelial Injury.Cardiovascular toxicology · 2025Review
- Mitochondrial Oxidative Stress and Vascular Remodeling in Uric Acid Nephropathy: Mechanistic Insights and Therapeutic Implications.International journal of nephrology and renovascular disease · 2025Review
- Receptor-Interacting Protein Kinase 3-Mediated Modulation of Endothelial Cell Necroptosis and Mitochondrial Dysfunction through AMPK/Drp1 Signaling Pathway: Insights into the Pathophysiological Mechanisms of Lipopolysaccharide-Induced Acute Lung Injury.International journal of medical sciences · 2025Article
- Glucose Metabolism Reprogramming of Vascular Endothelial Cells and Its Implication in Development of Atherosclerosis.Reviews in cardiovascular medicine · 2024Review
- Cytotoxic effects of the cigarette smoke extract of heated tobacco products on human oral squamous cell carcinoma: the role of reactive oxygen species and CaMKK2.The journal of physiological sciences : JPS · 2024Article
- The role and intervention of mitochondrial metabolism in osteoarthritis.Molecular and cellular biochemistry · 2024Review
- Metabolic Regulation of Endothelial Cells: A New Era for Treating Wet Age-Related Macular Degeneration.International journal of molecular sciences · 2024Review
- Mitochondrial quality control: a pathophysiological mechanism and potential therapeutic target for chronic obstructive pulmonary disease.Frontiers in pharmacology · 2024Review
- The Apelin/APJ System: A Potential Therapeutic Target for Sepsis.Journal of inflammation research · 2024Review
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
- Role of mitochondria in inflammatory lung diseases.Frontiers in pharmacology · 2024Review
- Association Between Systolic Blood Pressure and in-Hospital Mortality Among Congestive Heart Failure Patients with Chronic Obstructive Pulmonary Disease in the Intensive Care Unit: A Retrospective Cohort Study.International journal of chronic obstructive pulmonary disease · 2024Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Peroxinredoxin 6 reduction accelerates cigarette smoke extract‑induced senescence by regulating autophagy in BEAS‑2B cells.Experimental and therapeutic medicine · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a common disease characterized by persistent airflow limitation. Pulmonary vascular endothelial barrier injury and inflammation are increasingly considered to be important pathophysiological processes in cigarette smoke extract (CSE)-induced COPD, but the mechanism remains unclear. To identify the cellular mechanism of endothelial barrier injury and inflammation in CSE-treated human umbilical vein endothelial cells (HUVECs), we investigated the effect of the mitochondrion-targeting antioxidant mitoquinone (MitoQ) on endothelial barrier injury and inflammation. We demonstrated that MitoQ restored endothelial barrier integrity by preventing VE-cadherin disassembly and actin cytoskeleton remodeling, as well as decreased inflammation by the NF-κB and NLRP3 inflammasome pathways in endothelial cells. In addition, MitoQ also maintained mitochondrial function by reducing the production of ROS and excess autophagy. Inhibition of autophagy by 3-MA protected against cytotoxicity that was induced by CSE in HUVECs. Overall, our study indicated that mitochondrial damage is a key promoter in the induction of endothelial barrier dysfunction and inflammation by CSE. The protective effect of MitoQ is related to the inhibition of ROS and excess autophagy in CSE-induced HUVEC injury.
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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.