ArticleJournal of geriatric cardiology : JGC2015
The mitochondrial Na(+)/Ca(2+) exchanger may reduce high glucose-induced oxidative stress and nucleotide-binding oligomerization domain receptor 3 inflammasome activation in endothelial cells.
Article in Journal of geriatric cardiology : JGC, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Loss of TMEM65 in mice causes mitochondrial disease mediated by mitochondrial CaNature communications · 2026Article
- Mitochondria and Oxidative Stress as a Link between Alzheimer's Disease and Diabetes Mellitus.International journal of molecular sciences · 2023Review
- The role of Nod-like receptor protein 3 inflammasome activated by ion channels in multiple diseases.Molecular and cellular biochemistry · 2023Review
- Role of NLRP3 inflammasome in diabetes and COVID-19 role of NLRP3 inflammasome in the pathogenesis and treatment of COVID-19 and diabetes NLRP3 inflammasome in diabetes and COVID-19 intervention.Frontiers in immunology · 2023Review
- Astragalus Polysaccharides Reduce High-glucose-induced Rat Aortic Endothelial Cell Senescence and Inflammasome Activation by Modulating the Mitochondrial NaCell biochemistry and biophysics · 2022Article
- Pitavastatin activates mitophagy to protect EPC proliferation through a calcium-dependent CAMK1-PINK1 pathway in atherosclerotic mice.Communications biology · 2022Article
- Involvement of oxidative species in cyclosporine-mediated cholestasis.Frontiers in pharmacology · 2022Review
- Spotlight on NLRP3 Inflammasome: Role in Pathogenesis and Therapies of Atherosclerosis.Journal of inflammation research · 2021Review
- Mitochondrial Dysfunction in Chronic Respiratory Diseases: Implications for the Pathogenesis and Potential Therapeutics.Oxidative medicine and cellular longevity · 2021Review
- Diabetes Mellitus, Mitochondrial Dysfunction and CaInternational journal of molecular sciences · 2020Review
- Review
- Modulatory Mechanisms of the NLRP3 Inflammasomes in Diabetes.Biomolecules · 2019Review
- Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications.Frontiers in physiology · 2018Article
- NLRP3 Inflammasome as a Molecular Marker in Diabetic Cardiomyopathy.Frontiers in physiology · 2017Review
- Contribution of redox-dependent activation of endothelial Nlrp3 inflammasomes to hyperglycemia-induced endothelial dysfunction.Journal of molecular medicine (Berlin, Germany) · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mitochondrial Na(+)/Ca(2+) exchanger, NCLX, plays an important role in the balance between Ca(2+) influx and efflux across the mitochondrial inner membrane in endothelial cells. Mitochondrial metabolism is likely to be affected by the activity of NCLX because Ca(2+) activates several enzymes of the Krebs cycle. It is currently believed that mitochondria are not only centers of energy production but are also important sites of reactive oxygen species (ROS) generation and nucleotide-binding oligomerization domain receptor 3 (NLRP3) inflammasome activation. METHODS &
resultsThis study focused on NCLX function, in rat aortic endothelial cells (RAECs), induced by glucose. First, we detected an increase in NCLX expression in the endothelia of rats with diabetes mellitus, which was induced by an injection of streptozotocin. Next, colocalization of NCLX expression and mitochondria was detected using confocal analysis. Suppression of NCLX expression, using an siRNA construct (siNCLX), enhanced mitochondrial Ca(2+) influx and blocked efflux induced by glucose. Unexpectedly, silencing of NCLX expression induced increased ROS generation and NLRP3 inflammasome activation.
conclusionsThese findings suggest that NCLX affects glucose-dependent mitochondrial Ca(2+) signaling, thereby regulating ROS generation and NLRP3 inflammasome activation in high glucose conditions. In the early stages of high glucose stimulation, NCLX expression increases to compensate in order to self-protect mitochondrial maintenance, stability, and function in endothelial cells.
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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.