咖啡酸衍生物 MPMCA 可抑制破骨细胞生成并促进破骨细胞凋亡:对治疗骨质疏松疾病的启示

IF 3.9 3区 医学 Q2 CELL BIOLOGY Aging-Us Pub Date : 2024-08-26 DOI:10.18632/aging.206067
Le Huynh Hoai Thuong, Chin-Jung Hsu, Hsien-Te Chen, Yueh-Hsiung Kuo, Chih-Hsin Tang
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引用次数: 0

摘要

破骨细胞的活动在骨质疏松症和骨重塑的病理机制中起着至关重要的作用。治疗这些疾病的方法包括使用通过抑制破骨细胞活性发挥作用的药物。然而,目前的抗骨吸收和骨同化治疗普遍存在不良后果,而且不经常发生,这就造成了很大的弊端,因此限制了患者,尤其是老年人和/或患有多种疾病的患者长期服用这些药物。我们目前正在开发一种名为 N-(4-甲氧基苯)甲基咖啡酰胺(MPMCA)的新分子,它是咖啡酸的一种衍生物。这种化合物在阻止破骨细胞生成和使现有破骨细胞凋亡方面具有潜力。我们的研究发现,MPMCA 通过抑制 MAPK 通路来阻碍破骨细胞的功能。我们希望这项研究的结果能促进治疗抗骨质吸收的新方法的发展。
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Caffeic acid derivative MPMCA suppresses osteoclastogenesis and facilitates osteoclast apoptosis: implications for the treatment of bone loss disorders.

Osteoclast activity plays a crucial role in the pathological mechanisms of osteoporosis and bone remodeling. The treatment of these disorders involves the use of pharmacological medicines that work by inhibiting the activity of osteoclasts. Nevertheless, the prevalent and infrequent negative consequences of current antiresorptive and bone anabolic treatments pose significant drawbacks, hence restricting their prolonged administration in patients, particularly those who are elderly and/or suffer from many medical conditions. We are currently in the process of creating a new molecule called N-(4-methoxyphen) methyl caffeamide (MPMCA), which is a derivative of caffeic acid. This compound has shown potential in preventing the production of osteoclasts and causing existing osteoclasts to undergo cell apoptosis. Our investigation discovered that MPMCA hinders osteoclast function via suppressing the MAPK pathways. The expectation is that the findings of this study will stimulate the advancement of a novel approach to treating anti-resorption.

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来源期刊
Aging-Us
Aging-Us CELL BIOLOGY-
CiteScore
10.00
自引率
0.00%
发文量
595
审稿时长
6-12 weeks
期刊介绍: Information not localized
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