摘要
骨质疏松症是一个重大的健康问题,能导致骨折引起死亡,美国有超过1000万人患有此病。正常骨的成骨细胞和破骨细胞的代谢作用合成作用之间保持着平衡。大多数骨质疏松治疗抑制破骨细胞的活性,甲状旁腺激素是唯一FDA批准的增加成骨细胞的活性的药物,但其疗效随着时间延长而减弱,寻找新的骨合成代谢剂十分重要。在体内产生一氧化氮(NO)的硝酸盐,能预防雌激素缺乏的啮齿类动物的骨损失。临床研究表明,硝酸盐有益于绝经后骨质疏松症。本文究了骨细胞中NO的来源和NO合成的调节,讨论了NO对成骨细胞和破骨细胞系细胞之间的影响,总结了体内NO对骨骼影响的临床前和临床数据。因为NO对合成代谢和抗骨吸收作用的影响,新型NO供体和其他提高NO的产生和体内生物利用度方法可能是新的治疗骨质疏松症的方法。
关键词: 骨质疏松,骨细胞,新骨形成促进剂。
Current Medicinal Chemistry
Title:Targeting NO Signaling for the Treatment of Osteoporosis
Volume: 23 Issue: 24
Author(s): Hema Kalyanaraman, Ghania Ramdani, Renate B. Pilz
Affiliation:
关键词: 骨质疏松,骨细胞,新骨形成促进剂。
摘要: Osteoporosis is a major health problem, affecting over 10 million people in the U.S. and leading to fractures associated with significant morbidity and mortality. Normal bone mass is maintained by a balance between the anabolic effects of osteoblasts and catabolic effects of osteoclasts. Most osteoporosis therapies inhibit osteoclast activity; parathyroid hormone is the only FDA-approved agent that increases osteoblast activity, but its efficacy wanes over time, and there is a need for novel bone-anabolic agents. Nitrates, which generate nitric oxide (NO) in vivo, prevent bone loss from estrogen-deficiency in rodents, and some clinical data suggest beneficial effects of nitrates in post-menopausal osteoporosis. Here, we examine the sources of NO and regulation of NO synthesis in bone cells, review the effects of NO in cells of osteoblastic and osteoclastic lineage, and summarize existing preclinical and clinical data to document the skeletal effects of NO in vivo. Based on the anabolic and anti-resorptive effects of NO in bone, novel NO donors and other strategies to enhance NO production and bioavailability in vivo may represent a new treatment strategy for osteoporosis.
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Cite this article as:
Hema Kalyanaraman, Ghania Ramdani, Renate B. Pilz , Targeting NO Signaling for the Treatment of Osteoporosis, Current Medicinal Chemistry 2016; 23 (24) . https://dx.doi.org/10.2174/0929867323666160805123422
DOI https://dx.doi.org/10.2174/0929867323666160805123422 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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