摘要
Objective： Coronary artery calcification （CAC） is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure （CRF）, CAC is very common, and CAC severity correlates with the deterioration of renal lilnction. We summarized the current understanding and emerging findings of the relationship between CAC and CRF. Data Sources： All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms ＂coronary calcification＂, ＂＇chronic renal failure＂, ＇~vascular smooth muscle cell＂, and their synonyms until September 2017. Study Selection： We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies. Results： CRF can accelerate CAC progression. CRF increases the expression of pro-inflamrnatory factors, electrolyte imbalance （e.g., of calcium, phosphorus）, parathyroid hon^none, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transtbrm into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC. Conclusions： Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.
Objective： Coronary artery calcification （CAC） is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure （CRF）, CAC is very common, and CAC severity correlates with the deterioration of renal lilnction. We summarized the current understanding and emerging findings of the relationship between CAC and CRF. Data Sources： All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms ＂coronary calcification＂, ＂＇chronic renal failure＂, ＇~vascular smooth muscle cell＂, and their synonyms until September 2017. Study Selection： We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies. Results： CRF can accelerate CAC progression. CRF increases the expression of pro-inflamrnatory factors, electrolyte imbalance （e.g., of calcium, phosphorus）, parathyroid hon^none, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transtbrm into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC. Conclusions： Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.
基金
This study was supported by a grant from the National Natural Science Foundation of China （No. 81573732）.
