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Dludla, P.V.* ; Nkambule, B.B.* ; Tiano, L.* ; Louw, J.* ; Jastroch, M. ; Mazibuko-Mbeje, S.E.*

Uncoupling proteins as a therapeutic target to protect the diabetic heart.

Pharmacol. Res. 137, 11-24 (2018)
Postprint DOI PMC
Open Access Green
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Cardiomyopathy ; Diabetes Mellitus ; Oxidative Stress ; Uncoupling Proteins
Sprache
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 1043-6618
e-ISSN 1096-1186
Quellenangaben Band: 137, Heft: , Seiten: 11-24 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-221
Scopus ID 85053830639
PubMed ID 30223086
Erfassungsdatum 2018-09-27