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Uncoupling proteins as a therapeutic target to protect the diabetic heart
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Number of Authors: 62018 (English)In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 137, p. 11-24Article, review/survey (Refereed) Published
Abstract [en]

Myocardial remodeling and dysfunction caused by accelerated oxidative damage is a widely reported phenomenon within a diabetic state. Altered myocardial substrate preference appears to be the major cause of enhanced oxidative stress-mediated cell injury within a diabetic heart. During this process, exacerbated free fatty acid flux causes an abnormal increase in mitochondrial membrane potential leading to the overproduction of free radical species and subsequent cell damage. Uncoupling proteins (UCPs) are expressed within the myocardium and can protect against free radical damage by modulating mitochondrial respiration, leading to reduced production of reactive oxygen species. Moreover, transgenic animals lacking UCPs have been shown to be more susceptible to oxidative damage and display reduced cardiac function when compared to wild type animals. This suggests that tight regulation of UCPs is necessary for normal cardiac function and in the prevention of diabetes-induced oxidative damage. This review aims to enhance our understanding of the pathophysiological mechanisms relating to the role of UCPs in a diabetic heart, and further discuss known pharmacological compounds and hormones that can protect a diabetic heart through the modulation of UCPs.

Place, publisher, year, edition, pages
2018. Vol. 137, p. 11-24
Keywords [en]
Diabetes mellitus, Cardiomyopathy, Oxidative stress, Uncoupling proteins
National Category
Endocrinology and Diabetes Cardiac and Cardiovascular Systems
Identifiers
URN: urn:nbn:se:su:diva-162878DOI: 10.1016/j.phrs.2018.09.013ISI: 000451356100002PubMedID: 30223086OAI: oai:DiVA.org:su-162878DiVA, id: diva2:1274115
Available from: 2018-12-28 Created: 2018-12-28 Last updated: 2018-12-28Bibliographically approved

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Jastroch, Martin
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Department of Molecular Biosciences, The Wenner-Gren Institute
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