Université Côte d'Azur, CHU, INSERM, C3M, 06204 Nice, France.
Université Côte d'Azur, INSERM, C3M, 06204 Nice, France.
Int J Mol Sci. 2021 Jun 17;22(12):6491. doi: 10.3390/ijms22126491.
Vascular calcification is defined as an inappropriate accumulation of calcium depots occurring in soft tissues, including the vascular wall. Growing evidence suggests that vascular calcification is an actively regulated process, sharing similar mechanisms with bone formation, implicating both inhibitory and inducible factors, mediated by osteoclast-like and osteoblast-like cells, respectively. This process, which occurs in nearly all the arterial beds and in both the medial and intimal layers, mainly involves vascular smooth muscle cells. In the vascular wall, calcification can have different clinical consequences, depending on the pattern, localization and nature of calcium deposition. Nuclear receptors are transcription factors widely expressed, activated by specific ligands that control the expression of target genes involved in a multitude of pathophysiological processes, including metabolism, cancer, inflammation and cell differentiation. Some of them act as drug targets. In this review we describe and discuss the role of different nuclear receptors in the control of vascular calcification.
血管钙化被定义为一种发生在软组织中的钙沉积异常积聚,包括血管壁。越来越多的证据表明,血管钙化是一个受调节的过程,与骨形成具有相似的机制,分别涉及破骨细胞样和成骨细胞样细胞的抑制和诱导因子。这个过程发生在几乎所有的动脉床中,以及中膜和内膜层,主要涉及血管平滑肌细胞。在血管壁中,钙化可根据钙沉积的模式、定位和性质产生不同的临床后果。核受体是广泛表达的转录因子,被特定的配体激活,这些配体控制着涉及多种病理生理过程(包括代谢、癌症、炎症和细胞分化)的靶基因的表达。其中一些作为药物靶点。在这篇综述中,我们描述并讨论了不同核受体在血管钙化调控中的作用。