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Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways
Hyperglycaemia, hypertension, dyslipidemia and insulin resistance collectively impact on the myocardium of people with diabetes, triggering molecular, structural and myocardial abnormalities. These have been suggested to aggravate oxidative stress, systemic inflammation, myocardial lipotoxicity and...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237289/ https://www.ncbi.nlm.nih.gov/pubmed/28086863 http://dx.doi.org/10.1186/s12933-016-0484-4 |
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author | Lew, Jason Kar Sheng Pearson, James T. Schwenke, Daryl O. Katare, Rajesh |
author_facet | Lew, Jason Kar Sheng Pearson, James T. Schwenke, Daryl O. Katare, Rajesh |
author_sort | Lew, Jason Kar Sheng |
collection | PubMed |
description | Hyperglycaemia, hypertension, dyslipidemia and insulin resistance collectively impact on the myocardium of people with diabetes, triggering molecular, structural and myocardial abnormalities. These have been suggested to aggravate oxidative stress, systemic inflammation, myocardial lipotoxicity and impaired myocardial substrate utilization. As a consequence, this leads to the development of a spectrum of cardiovascular diseases, which may include but not limited to coronary endothelial dysfunction, and left ventricular remodelling and dysfunction. Diabetic heart disease (DHD) is the term used to describe the presence of heart disease specifically in diabetic patients. Despite significant advances in medical research and long clinical history of anti-diabetic medications, the risk of heart failure in people with diabetes never declines. Interestingly, sustainable and long-term exercise regimen has emerged as an effective synergistic therapy to combat the cardiovascular complications in people with diabetes, although the precise molecular mechanism(s) underlying this protection remain unclear. This review provides an overview of the underlying mechanisms of hyperglycaemia- and insulin resistance-mediated DHD with a detailed discussion on the role of different intensities of exercise in mitigating these molecular alterations in diabetic heart. In particular, we provide the possible role of exercise on microRNAs, the key molecular regulators of several pathophysiological processes. |
format | Online Article Text |
id | pubmed-5237289 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-52372892017-01-18 Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways Lew, Jason Kar Sheng Pearson, James T. Schwenke, Daryl O. Katare, Rajesh Cardiovasc Diabetol Review Hyperglycaemia, hypertension, dyslipidemia and insulin resistance collectively impact on the myocardium of people with diabetes, triggering molecular, structural and myocardial abnormalities. These have been suggested to aggravate oxidative stress, systemic inflammation, myocardial lipotoxicity and impaired myocardial substrate utilization. As a consequence, this leads to the development of a spectrum of cardiovascular diseases, which may include but not limited to coronary endothelial dysfunction, and left ventricular remodelling and dysfunction. Diabetic heart disease (DHD) is the term used to describe the presence of heart disease specifically in diabetic patients. Despite significant advances in medical research and long clinical history of anti-diabetic medications, the risk of heart failure in people with diabetes never declines. Interestingly, sustainable and long-term exercise regimen has emerged as an effective synergistic therapy to combat the cardiovascular complications in people with diabetes, although the precise molecular mechanism(s) underlying this protection remain unclear. This review provides an overview of the underlying mechanisms of hyperglycaemia- and insulin resistance-mediated DHD with a detailed discussion on the role of different intensities of exercise in mitigating these molecular alterations in diabetic heart. In particular, we provide the possible role of exercise on microRNAs, the key molecular regulators of several pathophysiological processes. BioMed Central 2017-01-13 /pmc/articles/PMC5237289/ /pubmed/28086863 http://dx.doi.org/10.1186/s12933-016-0484-4 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Lew, Jason Kar Sheng Pearson, James T. Schwenke, Daryl O. Katare, Rajesh Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title | Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title_full | Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title_fullStr | Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title_full_unstemmed | Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title_short | Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways |
title_sort | exercise mediated protection of diabetic heart through modulation of microrna mediated molecular pathways |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237289/ https://www.ncbi.nlm.nih.gov/pubmed/28086863 http://dx.doi.org/10.1186/s12933-016-0484-4 |
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