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Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart

Diabetes is a chronic, endocrine disorder that effects millions of people worldwide. Cardiovascular complications are the major cause of diabetes-related morbidity and mortality. Cardiac β(1)- and β(2)-adrenoceptor (AR) stimulation mediates positive inotropy and chronotropy, whereas β(3)-AR mediates...

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Autores principales: Erdogan, Betul R., Michel, Martin C., Arioglu-Inan, Ebru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7759850/
https://www.ncbi.nlm.nih.gov/pubmed/33256212
http://dx.doi.org/10.3390/cells9122548
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author Erdogan, Betul R.
Michel, Martin C.
Arioglu-Inan, Ebru
author_facet Erdogan, Betul R.
Michel, Martin C.
Arioglu-Inan, Ebru
author_sort Erdogan, Betul R.
collection PubMed
description Diabetes is a chronic, endocrine disorder that effects millions of people worldwide. Cardiovascular complications are the major cause of diabetes-related morbidity and mortality. Cardiac β(1)- and β(2)-adrenoceptor (AR) stimulation mediates positive inotropy and chronotropy, whereas β(3)-AR mediates negative inotropic effect. Changes in β-AR responsiveness are thought to be an important factor that contributes to the diabetic cardiac dysfunction. Diabetes related changes in β-AR expression, signaling, and β-AR mediated cardiac function have been studied by several investigators for many years. In the present review, we have screened PubMed database to obtain relevant articles on this topic. Our search has ended up with wide range of different findings about the effect of diabetes on β-AR mediated changes both in molecular and functional level. Considering these inconsistent findings, the effect of diabetes on cardiac β-AR still remains to be clarified.
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spelling pubmed-77598502020-12-26 Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart Erdogan, Betul R. Michel, Martin C. Arioglu-Inan, Ebru Cells Review Diabetes is a chronic, endocrine disorder that effects millions of people worldwide. Cardiovascular complications are the major cause of diabetes-related morbidity and mortality. Cardiac β(1)- and β(2)-adrenoceptor (AR) stimulation mediates positive inotropy and chronotropy, whereas β(3)-AR mediates negative inotropic effect. Changes in β-AR responsiveness are thought to be an important factor that contributes to the diabetic cardiac dysfunction. Diabetes related changes in β-AR expression, signaling, and β-AR mediated cardiac function have been studied by several investigators for many years. In the present review, we have screened PubMed database to obtain relevant articles on this topic. Our search has ended up with wide range of different findings about the effect of diabetes on β-AR mediated changes both in molecular and functional level. Considering these inconsistent findings, the effect of diabetes on cardiac β-AR still remains to be clarified. MDPI 2020-11-26 /pmc/articles/PMC7759850/ /pubmed/33256212 http://dx.doi.org/10.3390/cells9122548 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
Erdogan, Betul R.
Michel, Martin C.
Arioglu-Inan, Ebru
Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title_full Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title_fullStr Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title_full_unstemmed Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title_short Expression and Signaling of β-Adrenoceptor Subtypes in the Diabetic Heart
title_sort expression and signaling of β-adrenoceptor subtypes in the diabetic heart
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7759850/
https://www.ncbi.nlm.nih.gov/pubmed/33256212
http://dx.doi.org/10.3390/cells9122548
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