دورية أكاديمية

Osteoblast lineage Sod2 deficiency leads to an osteoporosis-like phenotype in mice

التفاصيل البيبلوغرافية
العنوان: Osteoblast lineage Sod2 deficiency leads to an osteoporosis-like phenotype in mice
المؤلفون: Astrid M. Schoppa, Xiangxu Chen, Jan-Moritz Ramge, Anna Vikman, Verena Fischer, Melanie Haffner-Luntzer, Jana Riegger, Jan Tuckermann, Karin Scharffetter-Kochanek, Anita Ignatius
المصدر: Disease Models & Mechanisms, Vol 15, Iss 5 (2022)
بيانات النشر: The Company of Biologists, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine
LCC:Pathology
مصطلحات موضوعية: skeletal aging, osteoporosis, mitochondrial dysfunction, reactive oxygen species, senescence, Medicine, Pathology, RB1-214
الوصف: Osteoporosis is a systemic metabolic skeletal disease characterized by low bone mass and strength associated with fragility fractures. Oxidative stress, which results from elevated intracellular reactive oxygen species (ROS) and arises in the aging organism, is considered one of the critical factors contributing to osteoporosis. Mitochondrial (mt)ROS, as the superoxide anion (O2−) generated during mitochondrial respiration, are eliminated in the young organism by antioxidant defense mechanisms, including superoxide dismutase 2 (SOD2), the expression and activity of which are decreased in aging mesenchymal progenitor cells, accompanied by increased mtROS production. Using a mouse model of osteoblast lineage cells with Sod2 deficiency, we observed significant bone loss in trabecular and cortical bones accompanied by decreased osteoblast activity, increased adipocyte accumulation in the bone marrow and augmented osteoclast activity, suggestive of altered mesenchymal progenitor cell differentiation and osteoclastogenesis. Furthermore, osteoblast senescence was increased. To date, there are only a few studies suggesting a causal association between mtROS and cellular senescence in tissue in vivo. Targeting SOD2 to improve redox homeostasis could represent a potential therapeutic strategy for maintaining bone health during aging.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1754-8403
1754-8411
Relation: http://dmm.biologists.org/content/15/5/dmm049392; https://doaj.org/toc/1754-8403; https://doaj.org/toc/1754-8411
DOI: 10.1242/dmm.049392
URL الوصول: https://doaj.org/article/c8aec182ecca4e369874df7f5a60cafd
رقم الأكسشن: edsdoj.8aec182ecca4e369874df7f5a60cafd
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17548403
17548411
DOI:10.1242/dmm.049392