Autophagic predisposition in the insulin resistant diabetic heart

Mellor, Kimberley M., Reichelt, Melissa E. and Delbridge, Lea M. D. (2013) Autophagic predisposition in the insulin resistant diabetic heart. Life Sciences, 92 11: 616-620. doi:10.1016/j.lfs.2012.03.042


Author Mellor, Kimberley M.
Reichelt, Melissa E.
Delbridge, Lea M. D.
Title Autophagic predisposition in the insulin resistant diabetic heart
Journal name Life Sciences   Check publisher's open access policy
ISSN 0024-3205
1879-0631
Publication date 2013-03-28
Year available 2012
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.lfs.2012.03.042
Open Access Status Not yet assessed
Volume 92
Issue 11
Start page 616
End page 620
Total pages 5
Place of publication Philadelphia, PA, United States
Publisher Elsevier
Language eng
Abstract Existence of a diabetic cardiopathology, independent of vascular abnormalities, has been well reported. Diffuse interstitial fibrosis throughout the diabetic myocardium (even in the absence of an acute coronary event) suggests widespread cardiomyocyte attrition and cytokine activity. In addition to apoptotic and necrotic events, there is now good evidence that significant cardiomyocyte loss in the diabetic heart is driven by a different, non-apoptotic type of programmed cell death: autophagy. Although considered to be beneficial and pro-survival as a short term strategy to deal with acute stress, when chronically elevated or constitutive, excess autophagic activity has potential to be lethal. The insulin resistant myocardium exhibits various pro-autophagic characteristics: suppression of the PI3K(I)-Akt signaling pathway, oxidative stress and metabolic dysregulation, rendering the diabetic heart vulnerable to autophagic demise. There is compelling new evidence that in the diabetic myocardium cardiomyocyte attrition can be linked to autophagic upregulation.
Keyword Autophagy
Cardiac
Cell death
Diabetes
Insulin resistance
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: School of Chemistry and Molecular Biosciences
 
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