脂肪因子chemerin与骨质疏松症的关系展望

The perspective of the relationship between chemerin and osteoporosis

骨质疏松症是常见病、多发病,医学界对骨质疏松症发病机理与防治的研究愈显重要。近年研究表明,各种原因导致的骨量减少常伴有骨髓中脂肪组织含量的增加。骨质疏松的发生可能与骨代谢中成脂和成骨的比例有关。骨髓中脂肪组织在骨形成和造血支持中发挥重要作用,脂肪组织具有内分泌调节功能,释放出一系列重要的分泌性因子,比如:leptin、adiponectin、chemerin、resistin、visfatin等,在调节骨髓间充质干细胞向脂肪细胞分化过程中起关键作用。Chemerin是新发现的脂肪因子,它在免疫应答、脂质代谢、糖类代谢、炎症反应等生理病理过程中都起着重要的作用。它与leptin、adiponect等脂肪因子一样参与骨代谢的调节,对维持骨代谢的平衡起着重要的作用。Chemerin及其受体CMKLR1信号传递通路的激活可以调节骨髓间充质干细胞的分化,促进破骨细胞的生成,从而影响骨的重建。现在chemerin/CMKLR1信号通路影响骨代谢的作用机制还不是很明确,深入研究chemerin及其受体与骨质疏松的关系,可以进一步了解骨质疏松症发生机制,为治疗及预防骨质疏松症提供了新的方向。

Osteoporosis is one of the most common and frequently-occurring diseases.The research of the pathogenesis and prevention of osteoporosis become more important.In recent years, studies have shown that decrease of bone mass often accompanied with the increase of adiposite tissue in the bone marrow.The occurrence of osteoporosis may be related to the proportion of adipogenesis and osteogenesis in the bone metabolism.Bone marrow adipose tissue plays an important supporting role in bone formation and hematopoiesis.It has the endocrine function of releasing a series of important secretory factors, such as leptin, adiponectin, chemerin, resistin, visfatin, etc., in the regulation of adipocyte differentiation by bone marrow stormal cells （ BMSCs ） .Chemerin is a newly identified adipokine.It plays an important role in the immune respone, lipid metabolism, carbohydrate metabolism, inflammation, and other physiological and pathological processes.Chemerin as well as leptin and adiponectin are involved in the regulation of bone metabolism and in maintenance of the balance of bone metabolism.Activation of chemerin and its receptor CMKLR1 signal pathway may regulates the differentiation of BMSCs, stimulates the formation of osteoblasts, and further affects bone remodeling.The mechanism of the effect of chemerin/CMKLR1 signal pathway on bone metabolism is not clear.In-depth study of the relation between chemerin of osteoporosis may further understand the pathogenesis of osteoporosis, and provide new ways for treatment and prevention of the disease.