Mandal Chandi C
Department of Biochemistry, School of Life Sciences, Central University of Rajasthan , Rajasthan , India.
Front Endocrinol (Lausanne). 2015 Oct 23;6:165. doi: 10.3389/fendo.2015.00165. eCollection 2015.
Many epidemiological studies show a positive connection between cardiovascular diseases and risk of osteoporosis, suggesting a role of hyperlipidemia and/or hypercholesterolemia in regulating osteoporosis. The majority of the studies indicated a correlation between high cholesterol and high LDL-cholesterol level with low bone mineral density, a strong predictor of osteoporosis. Similarly, bone metastasis is a serious complication of cancer for patients. Several epidemiological and basic studies have established that high cholesterol is associated with increased cancer risk. Moreover, osteoporotic bone environment predisposes the cancer cells for metastatic growth in the bone microenvironment. This review focuses on how cholesterol and cholesterol-lowering drugs (statins) regulate the functions of bone residential osteoblast and osteoclast cells to augment or to prevent bone deterioration. Moreover, this study provides an insight into molecular mechanisms of cholesterol-mediated bone deterioration. It also proposes a potential mechanism by which cellular cholesterol boosts cancer-induced bone metastasis.
许多流行病学研究表明,心血管疾病与骨质疏松风险之间存在正相关,提示高脂血症和/或高胆固醇血症在调节骨质疏松中发挥作用。大多数研究表明,高胆固醇和高LDL-胆固醇水平与低骨矿物质密度相关,而低骨矿物质密度是骨质疏松的一个强有力预测指标。同样,骨转移是癌症患者的一种严重并发症。多项流行病学和基础研究已证实,高胆固醇与癌症风险增加有关。此外,骨质疏松的骨环境使癌细胞易于在骨微环境中发生转移生长。本综述重点关注胆固醇和降胆固醇药物(他汀类药物)如何调节骨驻留成骨细胞和破骨细胞的功能,以增强或预防骨质恶化。此外,本研究深入探讨了胆固醇介导的骨质恶化的分子机制。它还提出了一种细胞胆固醇促进癌症诱导的骨转移的潜在机制。