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Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes
The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071562/ https://www.ncbi.nlm.nih.gov/pubmed/32169071 http://dx.doi.org/10.1186/s12933-020-01009-4 |
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author | Tang, Ying Li, Sheng-Lan Hu, Jia-Hui Sun, Kai-Jun Liu, Lei-Ling Xu, Dan-Yan |
author_facet | Tang, Ying Li, Sheng-Lan Hu, Jia-Hui Sun, Kai-Jun Liu, Lei-Ling Xu, Dan-Yan |
author_sort | Tang, Ying |
collection | PubMed |
description | The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via a variety of non-classical mechanisms that involve lysosomal, inflammatory, apoptotic, mitochondrial, and immune pathways. In this review paper, we summarized these additional mechanisms and described how anti-PCSK9 therapy exerts effects through these mechanisms. These additional pathways further illustrate the regulatory role of PCSK9 in atherosclerosis and offer an in-depth interpretation of how the PCSK9 inhibitor exerts effects on the treatment of atherosclerosis. |
format | Online Article Text |
id | pubmed-7071562 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-70715622020-03-18 Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes Tang, Ying Li, Sheng-Lan Hu, Jia-Hui Sun, Kai-Jun Liu, Lei-Ling Xu, Dan-Yan Cardiovasc Diabetol Review The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via a variety of non-classical mechanisms that involve lysosomal, inflammatory, apoptotic, mitochondrial, and immune pathways. In this review paper, we summarized these additional mechanisms and described how anti-PCSK9 therapy exerts effects through these mechanisms. These additional pathways further illustrate the regulatory role of PCSK9 in atherosclerosis and offer an in-depth interpretation of how the PCSK9 inhibitor exerts effects on the treatment of atherosclerosis. BioMed Central 2020-03-13 /pmc/articles/PMC7071562/ /pubmed/32169071 http://dx.doi.org/10.1186/s12933-020-01009-4 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Tang, Ying Li, Sheng-Lan Hu, Jia-Hui Sun, Kai-Jun Liu, Lei-Ling Xu, Dan-Yan Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title | Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title_full | Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title_fullStr | Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title_full_unstemmed | Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title_short | Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes |
title_sort | research progress on alternative non-classical mechanisms of pcsk9 in atherosclerosis in patients with and without diabetes |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071562/ https://www.ncbi.nlm.nih.gov/pubmed/32169071 http://dx.doi.org/10.1186/s12933-020-01009-4 |
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