Department of Comparative Biomedical Sciences, Royal Veterinary College, London, UK.
J Endocrinol. 2021 Feb;248(2):R51-R65. doi: 10.1530/JOE-20-0428.
Biomineralisation, the deposition of mineral onto a matrix, can be both a physiological and pathological process. Bone formation involves the secretion of an extracellular matrix (ECM) by osteoblasts and subsequent mineralisation of that matrix. It is regulated by a number of local and systemic factors and is necessary for maintenance of normal bone health. Conversely, mineralisation (or calcification) of soft tissues, including the vasculature, is detrimental to that tissue, leading to diseases such as arterial medial calcification (AMC). The mechanisms underlying AMC development are not fully defined, though it is thought that vascular smooth muscle cells (VSMCs) drive this complex, cell-mediated process. Similarly, AMC is regulated by a variety of enzymes and molecules, many of which have already been implicated in the regulation of bone mineralisation. This review will provide an overview of the similar, and sometimes opposing effects of these signalling molecules on the regulation of bone mineralisation and AMC.
生物矿化是指矿物质在基质上的沉积,它既可以是生理过程,也可以是病理过程。骨形成涉及成骨细胞分泌细胞外基质(ECM),随后 ECM 矿化。这一过程受到许多局部和全身因素的调节,对于维持正常的骨骼健康是必要的。相反,包括脉管系统在内的软组织矿化(或钙化)对该组织是有害的,导致动脉中层钙化(AMC)等疾病。尽管人们认为血管平滑肌细胞(VSMCs)驱动着这个复杂的、细胞介导的过程,但 AMC 发病机制尚未完全确定。同样,AMC 也受到多种酶和分子的调节,其中许多已经涉及到骨矿化的调节。本综述将概述这些信号分子在调节骨矿化和 AMC 方面的相似(有时是相反)作用。