骨质疏松症的肾素-血管紧张素系统发生机制及治疗靶点研究进展
发布时间:2018-01-17 17:28
本文关键词:骨质疏松症的肾素-血管紧张素系统发生机制及治疗靶点研究进展 出处:《中国药理学与毒理学杂志》2016年10期 论文类型:期刊论文
更多相关文章: 肾素-血管紧张素系统 骨质疏松症 骨代谢
【摘要】:骨质疏松症(OP)是一种骨代谢疾病,表现为骨形成减少和骨吸收增加,导致骨量丢失、骨组织微结构破坏,全身各处易于骨折。骨组织局部可表达肾素-血管紧张素系统(RAS)的主要成分并通过经典及非经典途径参与细胞氧化应激、增殖、分化及凋亡等过程。骨组织局部RAS过度激活时,一方面可以抑制成骨细胞分化或直接损伤其骨形成功能,另一方面促进破骨细胞分化和成熟,二者共同导致骨形成减少、骨吸收增加,参与OP发生。RAS抑制剂包括肾素抑制剂、血管紧张素转换酶抑制剂和血管紧张素Ⅱ受体拮抗剂,已经被证实可以有效地拮抗RAS慢性激活时产生的病理效应,因此被认为是治疗OP的候选药物之一。
[Abstract]:Osteoporosis (Osteoporosis) is a kind of bone metabolic disease, which is characterized by reduced bone formation and increased bone resorption, resulting in loss of bone mass and destruction of bone microstructure. Bone tissue can express the main components of renin-angiotensin system (Ras) and participate in cell oxidative stress and proliferation through classical and non-classical approaches. During the process of differentiation and apoptosis, local RAS can inhibit the differentiation of osteoblasts or directly damage the bone formation function, on the other hand, promote the differentiation and maturation of osteoclasts. Both of them lead to decrease of bone formation and increase of bone resorption. Ras inhibitors include renin inhibitor angiotensin converting enzyme inhibitor and angiotensin 鈪,
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