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Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy

Diabetic cardiomyopathy (DCM) or diabetes-induced cardiac dysfunction is a direct consequence of uncontrolled metabolic syndrome and is widespread in US population and worldwide. Despite of the heterogeneous and distinct features of DCM, the clinical relevance of DCM is now becoming established. DCM...

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Detalles Bibliográficos
Autores principales: Kain, Vasundhara, Halade, Ganesh V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449449/
https://www.ncbi.nlm.nih.gov/pubmed/28620607
http://dx.doi.org/10.3389/fcvm.2017.00031
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author Kain, Vasundhara
Halade, Ganesh V.
author_facet Kain, Vasundhara
Halade, Ganesh V.
author_sort Kain, Vasundhara
collection PubMed
description Diabetic cardiomyopathy (DCM) or diabetes-induced cardiac dysfunction is a direct consequence of uncontrolled metabolic syndrome and is widespread in US population and worldwide. Despite of the heterogeneous and distinct features of DCM, the clinical relevance of DCM is now becoming established. DCM progresses to pathological cardiac remodeling with the higher risk of heart attack and subsequent heart failure in diabetic patients. In this review, we emphasize lipid substrate quality and the phenotypic, metabolic, and biochemical stressors of DCM in the rodent and human pathophysiology. We discuss lipoxygenase signaling in the inflammatory pathway with multiple contributing and confounding factors leading to DCM. Additionally, emerging biochemical pathways are emphasized to make progress toward therapeutic advancement to treat DCM.
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spelling pubmed-54494492017-06-15 Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy Kain, Vasundhara Halade, Ganesh V. Front Cardiovasc Med Cardiovascular Medicine Diabetic cardiomyopathy (DCM) or diabetes-induced cardiac dysfunction is a direct consequence of uncontrolled metabolic syndrome and is widespread in US population and worldwide. Despite of the heterogeneous and distinct features of DCM, the clinical relevance of DCM is now becoming established. DCM progresses to pathological cardiac remodeling with the higher risk of heart attack and subsequent heart failure in diabetic patients. In this review, we emphasize lipid substrate quality and the phenotypic, metabolic, and biochemical stressors of DCM in the rodent and human pathophysiology. We discuss lipoxygenase signaling in the inflammatory pathway with multiple contributing and confounding factors leading to DCM. Additionally, emerging biochemical pathways are emphasized to make progress toward therapeutic advancement to treat DCM. Frontiers Media S.A. 2017-05-31 /pmc/articles/PMC5449449/ /pubmed/28620607 http://dx.doi.org/10.3389/fcvm.2017.00031 Text en Copyright © 2017 Kain and Halade. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cardiovascular Medicine
Kain, Vasundhara
Halade, Ganesh V.
Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title_full Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title_fullStr Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title_full_unstemmed Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title_short Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy
title_sort metabolic and biochemical stressors in diabetic cardiomyopathy
topic Cardiovascular Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449449/
https://www.ncbi.nlm.nih.gov/pubmed/28620607
http://dx.doi.org/10.3389/fcvm.2017.00031
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