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Peripheral Biomarker for Vascular Disorders

Atherosclerosis is the underlying cause of most myocardial infarction (MI) and ischaemic stroke episodes. An early sign of atherosclerosis is hypertrophy of the arterial wall. It is known that increased intima media thickness (IMT) is a non-invasive marker of arterial wall alteration, which can easi...

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Autores principales: Shad, Kaneez Fatima, Luqman, Nazar, Simpson, Ann M, Lal, Sara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287300/
https://www.ncbi.nlm.nih.gov/pubmed/30546256
http://dx.doi.org/10.1177/1177271918812467
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author Shad, Kaneez Fatima
Luqman, Nazar
Simpson, Ann M
Lal, Sara
author_facet Shad, Kaneez Fatima
Luqman, Nazar
Simpson, Ann M
Lal, Sara
author_sort Shad, Kaneez Fatima
collection PubMed
description Atherosclerosis is the underlying cause of most myocardial infarction (MI) and ischaemic stroke episodes. An early sign of atherosclerosis is hypertrophy of the arterial wall. It is known that increased intima media thickness (IMT) is a non-invasive marker of arterial wall alteration, which can easily be assessed in the carotid arteries by high-resolution B-mode ultrasound. Similarly, the other key element of MI and ischaemic strokes is the N-methyl-D-aspartate (NMDA) receptor which is an ionotropic glutamate receptor that mediates the vast majority of excitatory neurotransmission in the brain. NMDA activation requires the binding of both glutamate and a coagonist like D-serine to its glycine site. A special enzyme, serine racemase (SR), is required for the conversion of L-serine into D-serine, and alterations in SR activities lead to a variety of physiological and pathological conditions ranging from synaptic plasticity to ischemia, MI, and stroke. The amount of D-serine available for the activation of glutamatergic signalling is largely determined by SR and we have developed ways to estimate its levels in human blood samples and correlate it with the IMT. This research based short communication describes our pilot study, which clearly suggests that there is a direct relationship between the SR, D-serine, and IMT. In this article, we will discuss whether the activity of SR can determine the future consequences resulting from vascular pathologies such as MI and stroke.
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spelling pubmed-62873002018-12-13 Peripheral Biomarker for Vascular Disorders Shad, Kaneez Fatima Luqman, Nazar Simpson, Ann M Lal, Sara Biomark Insights Short Report Atherosclerosis is the underlying cause of most myocardial infarction (MI) and ischaemic stroke episodes. An early sign of atherosclerosis is hypertrophy of the arterial wall. It is known that increased intima media thickness (IMT) is a non-invasive marker of arterial wall alteration, which can easily be assessed in the carotid arteries by high-resolution B-mode ultrasound. Similarly, the other key element of MI and ischaemic strokes is the N-methyl-D-aspartate (NMDA) receptor which is an ionotropic glutamate receptor that mediates the vast majority of excitatory neurotransmission in the brain. NMDA activation requires the binding of both glutamate and a coagonist like D-serine to its glycine site. A special enzyme, serine racemase (SR), is required for the conversion of L-serine into D-serine, and alterations in SR activities lead to a variety of physiological and pathological conditions ranging from synaptic plasticity to ischemia, MI, and stroke. The amount of D-serine available for the activation of glutamatergic signalling is largely determined by SR and we have developed ways to estimate its levels in human blood samples and correlate it with the IMT. This research based short communication describes our pilot study, which clearly suggests that there is a direct relationship between the SR, D-serine, and IMT. In this article, we will discuss whether the activity of SR can determine the future consequences resulting from vascular pathologies such as MI and stroke. SAGE Publications 2018-11-29 /pmc/articles/PMC6287300/ /pubmed/30546256 http://dx.doi.org/10.1177/1177271918812467 Text en © The Author(s) 2018 http://www.creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Short Report
Shad, Kaneez Fatima
Luqman, Nazar
Simpson, Ann M
Lal, Sara
Peripheral Biomarker for Vascular Disorders
title Peripheral Biomarker for Vascular Disorders
title_full Peripheral Biomarker for Vascular Disorders
title_fullStr Peripheral Biomarker for Vascular Disorders
title_full_unstemmed Peripheral Biomarker for Vascular Disorders
title_short Peripheral Biomarker for Vascular Disorders
title_sort peripheral biomarker for vascular disorders
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287300/
https://www.ncbi.nlm.nih.gov/pubmed/30546256
http://dx.doi.org/10.1177/1177271918812467
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