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骨生物学中的血红素加氧酶-1:骨质疏松症的潜在治疗策略

HO-1 in Bone Biology: Potential Therapeutic Strategies for Osteoporosis.

作者信息

Zhou Xueman, Yuan Wenxiu, Xiong Xin, Zhang Zhenzhen, Liu Jiaqi, Zheng Yingcheng, Wang Jun, Liu Jin

机构信息

State Key Laboratory of Oral Diseases and National Clinical Research Center for West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Lab for Aging Research, State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China.

出版信息

Front Cell Dev Biol. 2021 Nov 30;9:791585. doi: 10.3389/fcell.2021.791585. eCollection 2021.

DOI:10.3389/fcell.2021.791585
PMID:34917622
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8669958/
Abstract

Osteoporosis is a prevalent bone disorder characterized by bone mass reduction and deterioration of bone microarchitecture leading to bone fragility and fracture risk. In recent decades, knowledge regarding the etiological mechanisms emphasizes that inflammation, oxidative stress and senescence of bone cells contribute to the development of osteoporosis. Studies have demonstrated that heme oxygenase 1 (HO-1), an inducible enzyme catalyzing heme degradation, exhibits anti-inflammatory, anti-oxidative stress and anti-apoptosis properties. Emerging evidence has revealed that HO-1 is critical in the maintenance of bone homeostasis, making HO-1 a potential target for osteoporosis treatment. In this Review, we aim to provide an introduction to current knowledge of HO-1 biology and its regulation, focusing specifically on its roles in bone homeostasis and osteoporosis. We also examine the potential of HO-1-based pharmacological therapeutics for osteoporosis and issues faced during clinical translation.

摘要

骨质疏松症是一种常见的骨骼疾病,其特征是骨量减少和骨微结构恶化,导致骨骼脆弱和骨折风险增加。近几十年来,关于病因机制的知识强调,骨细胞的炎症、氧化应激和衰老促成了骨质疏松症的发展。研究表明,血红素加氧酶1(HO-1)是一种催化血红素降解的诱导酶,具有抗炎、抗氧化应激和抗凋亡特性。新出现的证据表明,HO-1在维持骨稳态中起关键作用,使HO-1成为骨质疏松症治疗的潜在靶点。在本综述中,我们旨在介绍HO-1生物学及其调控的当前知识,特别关注其在骨稳态和骨质疏松症中的作用。我们还研究了基于HO-1的骨质疏松症药物治疗的潜力以及临床转化过程中面临的问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/dc730d60e908/fcell-09-791585-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/bd3727f5628e/fcell-09-791585-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/4afe593d6a93/fcell-09-791585-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/dc730d60e908/fcell-09-791585-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/bd3727f5628e/fcell-09-791585-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/4afe593d6a93/fcell-09-791585-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7885/8669958/dc730d60e908/fcell-09-791585-g003.jpg

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