Eren Esin, Ellidag Hamit Yasar, Aydin Ozgur, Yılmaz Necat
Biochemistry Laboratory, Antalya Public Health Center of Ministry of Health, Antalya, Turkey.
Central Laboratories of Antalya Education and Research Hospital of Ministry of Health, Antalya, Turkey.
Chonnam Med J. 2014 Dec;50(3):75-81. doi: 10.4068/cmj.2014.50.3.75. Epub 2014 Dec 17.
The association of postmenopausal osteoporosis (PMOP) with both atherosclerosis and vascular/valvular calcification is well known. Recently, ample evidence has suggested a common etiologic factor, namely, reduced HDL-associated paraoxonase 1 (PON1) activity, as a causative factor in the development of PMOP and cardiovascular disease (CVD). This common etiologic factor not only contributes to atherosclerotic diseases but also to PMOP following an almost identical mechanism including dysfunctional HDL and lipid oxidation. According to recent studies, lipid oxidation might improve osteoblastic transformation of vascular cells and obstruct such transformation in bone cells. The primary objective of this current review was to summarize the evidence revealing the role of HDL-associated PON1 enzyme in PMOP. Additionally, the review aimed to address some of the subjects that need further investigation in order to define whether hyperhomocysteinemia and sensitivity to lipid oxidation may be risk factors for PMOP.
绝经后骨质疏松症(PMOP)与动脉粥样硬化以及血管/瓣膜钙化之间的关联已广为人知。最近,大量证据表明存在一个共同的病因因素,即高密度脂蛋白(HDL)相关的对氧磷酶1(PON1)活性降低,这是PMOP和心血管疾病(CVD)发生发展的一个致病因素。这个共同的病因因素不仅导致动脉粥样硬化疾病,还通过几乎相同的机制导致PMOP,包括HDL功能失调和脂质氧化。根据最近的研究,脂质氧化可能促进血管细胞向成骨细胞的转化,并阻碍骨细胞的这种转化。本综述的主要目的是总结揭示HDL相关PON1酶在PMOP中作用的证据。此外,该综述旨在探讨一些需要进一步研究的课题,以确定高同型半胱氨酸血症和对脂质氧化的敏感性是否可能是PMOP的危险因素。