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Exposure to type 2 diabetes provokes mitochondrial impairment in apparently healthy human hearts

Cardiac mitochondrial alterations are suspected to play a key role in the development of diabetes-related heart failure as reported in some animal and few human studies in type 2 diabetes (1). It is yet unclear whether these alterations are induced by diabetes-related metabolic changes or develop se...

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Main Authors: Zweck, Elric (Author) , Scheiber, Daniel (Author) , Jelenik, Tomas (Author) , Bönner, Florian (Author) , Horn, Patrick (Author) , Pesta, Dominik (Author) , Schultheiss, Heinz-Peter (Author) , Boeken, Udo (Author) , Akhyari, Payam (Author) , Lichtenberg, Artur (Author) , Kelm, Malte (Author) , Roden, Michael (Author) , Westenfeld, Ralf (Author) , Szendrödi, Julia (Author)
Format: Article (Journal)
Language:English
Published: 2021
In: Diabetes care
Year: 2021, Volume: 44, Issue: 5, Pages: e82-e84
ISSN:1935-5548
DOI:10.2337/dc20-2255
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.2337/dc20-2255
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Author Notes:Elric Zweck, Daniel Scheiber, Tomas Jelenik, Florian Bönner, Patrick Horn, Dominik Pesta, Heinz-Peter Schultheiss, Udo Boeken, Payam Akhyari, Artur Lichtenberg, Malte Kelm, Michael Roden, Ralf Westenfeld, and Julia Szendroedi
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Summary:Cardiac mitochondrial alterations are suspected to play a key role in the development of diabetes-related heart failure as reported in some animal and few human studies in type 2 diabetes (1). It is yet unclear whether these alterations are induced by diabetes-related metabolic changes or develop secondary to other factors underlying heart failure including micro- and macrovascular disease. We hypothesized that 1) exposure to type 2 diabetes provokes myocardial mitochondrial impairment prior to apparent left ventricular heart failure in humans and 2) these mitochondrial alterations are accompanied by increased oxidative stress, edema, and intracellular inflammation.
Item Description:Gesehen am 28.02.2022
Physical Description:Online Resource
ISSN:1935-5548
DOI:10.2337/dc20-2255

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