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Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets

The carotid body (CB) is responsible for the peripheral chemoreflex by sensing blood gases and pH. The CB also appears to act as a peripheral sensor of metabolites and hormones, regulating the metabolism. CB malfunction induces aberrant chemosensory responses that culminate in the tonic overactivati...

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Detalles Bibliográficos
Autores principales: Kim, Lenise J., Polotsky, Vsevolod Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7404212/
https://www.ncbi.nlm.nih.gov/pubmed/32698380
http://dx.doi.org/10.3390/ijms21145117
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author Kim, Lenise J.
Polotsky, Vsevolod Y.
author_facet Kim, Lenise J.
Polotsky, Vsevolod Y.
author_sort Kim, Lenise J.
collection PubMed
description The carotid body (CB) is responsible for the peripheral chemoreflex by sensing blood gases and pH. The CB also appears to act as a peripheral sensor of metabolites and hormones, regulating the metabolism. CB malfunction induces aberrant chemosensory responses that culminate in the tonic overactivation of the sympathetic nervous system. The sympatho-excitation evoked by CB may contribute to the pathogenesis of metabolic syndrome, inducing systemic hypertension, insulin resistance and sleep-disordered breathing. Several molecular pathways are involved in the modulation of CB activity, and their pharmacological manipulation may lead to overall benefits for cardiometabolic diseases. In this review, we will discuss the role of the CB in the regulation of metabolism and in the pathogenesis of the metabolic dysfunction induced by CB overactivity. We will also explore the potential pharmacological targets in the CB for the treatment of metabolic syndrome.
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spelling pubmed-74042122020-08-11 Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets Kim, Lenise J. Polotsky, Vsevolod Y. Int J Mol Sci Review The carotid body (CB) is responsible for the peripheral chemoreflex by sensing blood gases and pH. The CB also appears to act as a peripheral sensor of metabolites and hormones, regulating the metabolism. CB malfunction induces aberrant chemosensory responses that culminate in the tonic overactivation of the sympathetic nervous system. The sympatho-excitation evoked by CB may contribute to the pathogenesis of metabolic syndrome, inducing systemic hypertension, insulin resistance and sleep-disordered breathing. Several molecular pathways are involved in the modulation of CB activity, and their pharmacological manipulation may lead to overall benefits for cardiometabolic diseases. In this review, we will discuss the role of the CB in the regulation of metabolism and in the pathogenesis of the metabolic dysfunction induced by CB overactivity. We will also explore the potential pharmacological targets in the CB for the treatment of metabolic syndrome. MDPI 2020-07-20 /pmc/articles/PMC7404212/ /pubmed/32698380 http://dx.doi.org/10.3390/ijms21145117 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kim, Lenise J.
Polotsky, Vsevolod Y.
Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title_full Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title_fullStr Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title_full_unstemmed Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title_short Carotid Body and Metabolic Syndrome: Mechanisms and Potential Therapeutic Targets
title_sort carotid body and metabolic syndrome: mechanisms and potential therapeutic targets
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7404212/
https://www.ncbi.nlm.nih.gov/pubmed/32698380
http://dx.doi.org/10.3390/ijms21145117
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