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Uncoupling proteins as a therapeutic target to protect the diabetic heart.
Pharmacol. Res. 137, 11-24 (2018)
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.
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Publication type
Article: Journal article
Document type
Review
Keywords
Cardiomyopathy ; Diabetes Mellitus ; Oxidative Stress ; Uncoupling Proteins
Language
Publication Year
2018
HGF-reported in Year
2018
ISSN (print) / ISBN
1043-6618
e-ISSN
1096-1186
Journal
Pharmacological Research
Quellenangaben
Volume: 137,
Pages: 11-24
Publisher
Elsevier
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-501900-221
Scopus ID
85053830639
PubMed ID
30223086
Erfassungsdatum
2018-09-27