Obesity and lipid metabolism in the development of osteoporosis (Review).

IF 5.7 3区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
International journal of molecular medicine Pub Date : 2024-07-01 Epub Date: 2024-05-31 DOI:10.3892/ijmm.2024.5385
Xiaochuan Wang, Chi Zhang, Guang Zhao, Keda Yang, Lin Tao
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引用次数: 0

Abstract

Osteoporosis is a common bone metabolic disease that causes a heavy social burden and seriously threatens life. Improving osteogenic capacity is necessary to correct bone mass loss in the treatment of osteoporosis. Osteoblasts are derived from the differentiation of bone marrow mesenchymal stem cells, a process that opposes adipogenic differentiation. The peroxisome proliferator‑activated receptor γ and Wnt/β‑catenin signaling pathways mediate the mutual regulation of osteogenesis and adipogenesis. Lipid substances play an important role in the occurrence and development of osteoporosis. The content and proportion of lipids modulate the activity of immunocytes, mainly macrophages, and the secretion of inflammatory factors, such as IL‑1, IL‑6 and TNF‑α. These inflammatory effectors increase the activity and promote the differentiation of osteoclasts, which leads to bone imbalance and stronger bone resorption. Obesity also decreases the activity of antioxidases and leads to oxidative stress, thereby inhibiting osteogenesis. The present review starts by examining the bidirectional differentiation of BM‑MSCs, describes in detail the mechanism by which lipids affect bone metabolism, and discusses the regulatory role of inflammation and oxidative stress in this process. The review concludes that a reasonable adjustment of the content and proportion of lipids, and the alleviation of inflammatory storms and oxidative damage induced by lipid imbalances, will improve bone mass and treat osteoporosis.

骨质疏松症发病过程中的肥胖和脂质代谢(综述)。
骨质疏松症是一种常见的骨代谢疾病,造成沉重的社会负担,严重威胁生命。在治疗骨质疏松症的过程中,提高成骨能力是纠正骨量丢失的必要条件。成骨细胞来源于骨髓间充质干细胞的分化,这一过程与成脂分化相反。过氧化物酶体增殖激活受体γ和Wnt/β-catenin信号通路介导成骨和成脂的相互调控。脂类物质在骨质疏松症的发生和发展中起着重要作用。脂质的含量和比例会调节免疫细胞(主要是巨噬细胞)的活性以及炎症因子(如 IL-1、IL-6 和 TNF-α)的分泌。这些炎症效应因子会增加破骨细胞的活性并促进破骨细胞的分化,从而导致骨质失衡和更强的骨吸收。肥胖还会降低抗氧化酶的活性,导致氧化应激,从而抑制骨生成。本综述从研究 BM-MSCs 的双向分化入手,详细描述了脂质影响骨代谢的机制,并讨论了炎症和氧化应激在这一过程中的调节作用。综述认为,合理调整脂质的含量和比例,缓解脂质失衡诱发的炎症风暴和氧化损伤,可改善骨量,治疗骨质疏松症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
International journal of molecular medicine
International journal of molecular medicine 医学-医学:研究与实验
CiteScore
12.30
自引率
0.00%
发文量
124
审稿时长
3 months
期刊介绍: The main aim of Spandidos Publications is to facilitate scientific communication in a clear, concise and objective manner, while striving to provide prompt publication of original works of high quality. The journals largely concentrate on molecular and experimental medicine, oncology, clinical and experimental cancer treatment and biomedical research. All journals published by Spandidos Publications Ltd. maintain the highest standards of quality, and the members of their Editorial Boards are world-renowned scientists.
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