| Literature DB >> 32945991 |
Haoran Huang1,2, Zhaohuai Li1,3, Yuyi Ruan1,4, Weijing Feng5,6, Jie Chen5, Xiaoxue Li1, Liu Ouyang1,5, Hui Huang7.
Abstract
Over the past decades, circadian rhythm has drawn a great attention in cardiovascular diseases. The expressions of rhythm genes fluctuate in accordance with the diurnal changes of vascular physiology, which highlights the pivotal effect of vascular clock. Recent researches show that the circadian clock can directly regulate the synthetic and secretory function of endothelial cells and phenotypic switch of vascular smooth muscle cells to adjust vascular relaxation and contraction. Importantly, dysfunction of vascular cells is involved in vascular calcification. Secretion of osteogenic cytokines and calcified vesicles in the vessel, osteogenic phenotype switch of vascular smooth muscle cells are all implicated in the calcification process. Moreover, circadian rhythm disorder can lead to abnormal hormone secretion, oxidative stress, inflammatory reaction, and autophagy, all of which should not be ignored in vascular calcification. Vascular senescence is another pathogenetic mechanism in vascular calcification. Accelerated vascular senescence may act as an important intermediate factor to promote vascular calcification in circadian rhythm disorders. In this review, we elaborate the potential effect of circadian rhythm disorder in vascular calcification and try to provide a new direction in the prevention of vascular calcification.Entities:
Keywords: Autophagy; Circadian rhythm; Hormones; Inflammation; Oxidative stress; Vascular calcification
Mesh:
Year: 2020 PMID: 32945991 DOI: 10.1007/s13105-020-00767-9
Source DB: PubMed Journal: J Physiol Biochem ISSN: 1138-7548 Impact factor: 4.158