The Role of Nonenzymatic Post-translational Protein Modifications in Uremic Vascular Calcification
Copyright © 2019 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved..
Considerable technological advances have enabled the identification and linkage of nonenzymatic post-translationally modified proteins to the pathogenesis of cardiovascular disease (CVD) in patients with kidney failure. Through processes such as the nonenzymatic carbamylation reaction as well as the formation of advanced glycation end products, we now know that protein modifications are invariably associated with the development of CVD beyond a mere epiphenomenon and this has become an important focus of nephrology research in recent years. Although the specific mechanisms by which protein modifications occurring in kidney failure that may contribute to CVD are diverse and include pathways such as inflammation and fibrosis, vascular calcification has emerged as a distinct pathological sequelae of protein modifications. In this review, we consider the biological mechanisms and clinical relevance of protein carbamylation and advanced glycation end products in CVD development with a focus on vascular calcification.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:26 |
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Enthalten in: |
Advances in chronic kidney disease - 26(2019), 6 vom: 12. Nov., Seite 427-436 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Lim, Kenneth [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 04.08.2020 Date Revised 01.11.2020 published: Print Citation Status MEDLINE |
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doi: |
10.1053/j.ackd.2019.10.001 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM304323039 |
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520 | |a Considerable technological advances have enabled the identification and linkage of nonenzymatic post-translationally modified proteins to the pathogenesis of cardiovascular disease (CVD) in patients with kidney failure. Through processes such as the nonenzymatic carbamylation reaction as well as the formation of advanced glycation end products, we now know that protein modifications are invariably associated with the development of CVD beyond a mere epiphenomenon and this has become an important focus of nephrology research in recent years. Although the specific mechanisms by which protein modifications occurring in kidney failure that may contribute to CVD are diverse and include pathways such as inflammation and fibrosis, vascular calcification has emerged as a distinct pathological sequelae of protein modifications. In this review, we consider the biological mechanisms and clinical relevance of protein carbamylation and advanced glycation end products in CVD development with a focus on vascular calcification | ||
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