PDF(Pubmed)
Abstract：
There has been interest in the connection between cardiovascular diseases and osteoporosis, both of which share hyperlipidemia as a common pathological basis. Osteoporosis is a progressive metabolic bone disease characterized by reduced bone mass, deteriorated bone microstructure, increased bone fragility and heightened risk of bone fractures. Dysfunction of osteoblastic cells, vital for bone formation, is induced by excessive internalization of lipids under hyperlipidemic conditions, forming the crux of hyperlipidemia-associated osteoporosis. Autophagy, a process fundamental to cell self-regulation, serves a critical role in osteoblastic cell function and bone formation. When activated by lipids, lipophagy inhibits osteoblastic cell differentiation in response to elevated lipid concentrations, resulting in reduced bone mass and osteoporosis. However, an in-depth understanding of the precise roles and mechanisms of lipophagy in the regulation of osteoblastic cell function is required. Study of the molecular mechanisms governing osteoblastic cell response to excessive lipids can result in a clearer understanding of osteoporosis; therefore, potential strategies for preventing hyperlipidemia-induced osteoporosis can be developed. The present review discusses recent progress in elucidating the molecular mechanisms of lipophagy in the regulation of osteoblastic cell function, offering insights into hyperlipidemia-induced osteoporosis.
摘要：
人们对心血管疾病和骨质疏松症之间的联系感兴趣，两者都有高脂血症作为共同的病理基础。骨质疏松症是一种进行性代谢性骨病，其特征是骨量减少，骨微结构恶化，骨脆性增加，骨折风险增加。成骨细胞功能障碍，对骨骼形成至关重要，在高脂血症条件下由脂质过度内在化诱导，形成高脂血症相关骨质疏松症的症结所在。自噬,细胞自我调节的基础过程，在成骨细胞功能和骨形成中起关键作用。当被脂质激活时，脂质吞噬抑制成骨细胞分化以响应脂质浓度升高，导致骨量减少和骨质疏松症。然而,需要深入了解脂质吞噬在调节成骨细胞功能中的确切作用和机制。研究成骨细胞对过度脂质反应的分子机制可以导致对骨质疏松症有更清晰的认识；因此，可以开发预防高脂血症引起的骨质疏松症的潜在策略.本文就近年来脂吞噬调节成骨细胞功能的分子机制的研究进展作一综述。提供对高脂血症引起的骨质疏松症的见解。
