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SIRT3 在骨质疏松症中的作用。

The Role of SIRT3 in the Osteoporosis.

机构信息

The Orthopaedic Center, Wenling First People's Hospital (The Affiliated Wenling Hospital of Wenzhou Medical University), Wenling, China.

Department of Cardiology, Wenling First People's Hospital (The Affiliated Wenling Hospital of Wenzhou Medical University), Wenling, China.

出版信息

Front Endocrinol (Lausanne). 2022 May 25;13:893678. doi: 10.3389/fendo.2022.893678. eCollection 2022.

DOI:10.3389/fendo.2022.893678
PMID:35692409
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9175005/
Abstract

SIRT3 is an NAD-dependent deacetylase in the mitochondria with an extensive ability to regulate mitochondrial morphology and function. It has been reported that SIRT3 participates in the occurrence and development of many aging-related diseases. Osteoporosis is a common aging-related disease characterized by decreased bone mass and fragility fractures, which has caused a huge burden on society. Current research shows that SIRT3 is involved in the physiological processes of senescence of bone marrow mesenchymal stem cells (BMSCs), differentiation of BMSCs and osteoclasts. However, the specific effects and mechanisms of SIRT3 in osteoporosis are not clear. In the current review, we elaborated on the physiological functions of SIRT3, the cell types involved in bone remodeling, and the role of SIRT3 in osteoporosis. Furthermore, it also provided a theoretical basis for SIRT3 as a therapeutic target for osteoporosis.

摘要

SIRT3 是一种依赖 NAD 的线粒体去乙酰化酶,具有广泛调节线粒体形态和功能的能力。据报道,SIRT3 参与了许多与衰老相关的疾病的发生和发展。骨质疏松症是一种常见的与衰老相关的疾病,其特征是骨量减少和脆性骨折,给社会带来了巨大的负担。目前的研究表明,SIRT3 参与骨髓间充质干细胞(BMSCs)衰老、BMSCs 和破骨细胞分化的生理过程。然而,SIRT3 在骨质疏松症中的具体作用和机制尚不清楚。在本综述中,我们详细阐述了 SIRT3 的生理功能、参与骨重塑的细胞类型以及 SIRT3 在骨质疏松症中的作用。此外,它还为 SIRT3 作为骨质疏松症的治疗靶点提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a98/9175005/5dd0518b03de/fendo-13-893678-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a98/9175005/5dd0518b03de/fendo-13-893678-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a98/9175005/5dd0518b03de/fendo-13-893678-g001.jpg

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