التفاصيل البيبلوغرافية
| العنوان: |
DataSheet_1_Mitochondrial dysfunction and metabolic reprogramming induce macrophage pro-inflammatory phenotype switch and atherosclerosis progression in aging.pdf |
| المؤلفون: |
Aleksandr E. Vendrov, Andrey Lozhkin, Takayuki Hayami, Julia Levin, Jamille Silveira Fernandes Chamon, Ahmed Abdel-Latif, Marschall S. Runge, Nageswara R. Madamanchi |
| سنة النشر: |
2024 |
| المجموعة: |
Frontiers: Figshare |
| مصطلحات موضوعية: |
Immunology, Applied Immunology (incl. Antibody Engineering, Xenotransplantation and T-cell Therapies), Autoimmunity, Cellular Immunology, Humoural Immunology and Immunochemistry, Immunogenetics (incl. Genetic Immunology), Innate Immunity, Transplantation Immunology, Tumour Immunology, Immunology not elsewhere classified, Genetic Immunology, Animal Immunology, Veterinary Immunology, NOX4 NADPH oxidase, mitochondrial dysfunction, macrophages, atherosclerosis, aging |
| الوصف: |
Introduction Aging increases the risk of atherosclerotic vascular disease and its complications. Macrophages are pivotal in the pathogenesis of vascular aging, driving inflammation and atherosclerosis progression. NOX4 (NADPH oxidase 4) expression increases with age, correlating with mitochondrial dysfunction, inflammation, and atherosclerosis. We hypothesized that the NOX4-dependent mitochondrial oxidative stress promotes aging-associated atherosclerosis progression by causing metabolic dysfunction and inflammatory phenotype switch in macrophages. Methods We studied atherosclerotic lesion morphology and macrophage phenotype in young (5-month-old) and aged (16-month-old) Nox4 -/- /Apoe -/- and Apoe -/- mice fed Western diet. Results Young Nox4 -/- /Apoe -/- and Apoe -/- mice had comparable aortic and brachiocephalic artery atherosclerotic lesion cross-sectional areas. Aged mice showed significantly increased lesion area compared with young mice. Aged Nox4 -/- /Apoe -/- had significantly lower lesion areas than Apoe-/- mice. Compared with Apoe-/- mice, atherosclerotic lesions in aged Nox4 -/- /Apoe -/- showed reduced cellular and mitochondrial ROS and oxidative DNA damage, lower necrotic core area, higher collagen content, and decreased inflammatory cytokine expression. Immunofluorescence and flow cytometry analysis revealed that aged Apoe -/- mice had a higher percentage of classically activated pro-inflammatory macrophages (CD38 + CD80 + ) in the lesions. Aged Nox4 -/- /Apoe -/- mice had a significantly higher proportion of alternatively activated pro-resolving macrophages (EGR2 + /CD163 + CD206 + ) in the lesions, with an increased CD38 + /EGR2 + cell ratio compared with Apoe -/- mice. Mitochondrial respiration assessment revealed impaired oxidative phosphorylation and increased glycolytic ATP production in macrophages from aged Apoe -/- mice. In contrast, macrophages from Nox4 -/- /Apoe -/- mice were less glycolytic and more aerobic, with preserved basal and maximal respiration and mitochondrial ATP ... |
| نوع الوثيقة: |
dataset |
| اللغة: |
unknown |
| Relation: |
https://figshare.com/articles/dataset/DataSheet_1_Mitochondrial_dysfunction_and_metabolic_reprogramming_induce_macrophage_pro-inflammatory_phenotype_switch_and_atherosclerosis_progression_in_aging_pdf/26074558 |
| DOI: |
10.3389/fimmu.2024.1410832.s001 |
| الاتاحة: |
https://doi.org/10.3389/fimmu.2024.1410832.s001
https://figshare.com/articles/dataset/DataSheet_1_Mitochondrial_dysfunction_and_metabolic_reprogramming_induce_macrophage_pro-inflammatory_phenotype_switch_and_atherosclerosis_progression_in_aging_pdf/26074558 |
| Rights: |
CC BY 4.0 |
| رقم الانضمام: |
edsbas.53C0DA96 |
| قاعدة البيانات: |
BASE |