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Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure
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 function. We summarized the...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5850680/ https://www.ncbi.nlm.nih.gov/pubmed/29483398 http://dx.doi.org/10.4103/0366-6999.226066 |
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author | Lai, Jun Akindavyi, Gael Fu, Qiang Li, Zhi-Liang Wang, Hui-Min Wen, Li-Hua |
author_facet | Lai, Jun Akindavyi, Gael Fu, Qiang Li, Zhi-Liang Wang, Hui-Min Wen, Li-Hua |
author_sort | Lai, Jun |
collection | PubMed |
description | 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 function. 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-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transform 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. |
format | Online Article Text |
id | pubmed-5850680 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-58506802018-03-21 Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure Lai, Jun Akindavyi, Gael Fu, Qiang Li, Zhi-Liang Wang, Hui-Min Wen, Li-Hua Chin Med J (Engl) Review Article 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 function. 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-inflammatory factors, electrolyte imbalance (e.g., of calcium, phosphorus), parathyroid hormone, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transform 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. Medknow Publications & Media Pvt Ltd 2018-03-05 /pmc/articles/PMC5850680/ /pubmed/29483398 http://dx.doi.org/10.4103/0366-6999.226066 Text en Copyright: © 2018 Chinese Medical Journal http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. |
spellingShingle | Review Article Lai, Jun Akindavyi, Gael Fu, Qiang Li, Zhi-Liang Wang, Hui-Min Wen, Li-Hua Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title | Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title_full | Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title_fullStr | Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title_full_unstemmed | Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title_short | Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure |
title_sort | research progress on the relationship between coronary artery calcification and chronic renal failure |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5850680/ https://www.ncbi.nlm.nih.gov/pubmed/29483398 http://dx.doi.org/10.4103/0366-6999.226066 |
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