title: Unbreak my heart: targeting mitochondrial autophagy in diabetic cardiomyopathy.
abstract: CONCLUSIONS
  Diabetes is strongly associated with increased incidence of heart disease and mortality due to development of diabetic cardiomyopathy. Even in the absence of cardiovascular disease, cardiomyopathy frequently arises in diabetic patients. Current treatment options for cardiomyopathy in diabetic patients are the same as for nondiabetic patients and do not address the causes underlying the loss of contractility.
  
  
  BACKGROUND
  Although there are numerous distinctions between Type 1 and Type 2 diabetes, recent evidence suggests that the two disease states converge on mitochondria as an epicenter for cardiomyocyte damage.
  
  
  RESULTS
  Accumulation of dysfunctional mitochondria contributes to cardiac tissue injury in both acute and chronic conditions. Removal of damaged mitochondria by macroautophagy, termed "mitophagy," is critical for maintaining cardiomyocyte health and contractility both under normal conditions and during stress. However, very little is known about the involvement of mitophagy in the pathogenesis of diabetic cardiomyopathy. A growing interest in this topic has given rise to a wave of publications that aim at deciphering the status of autophagy and mitophagy in Type 1 and Type 2 diabetes.
  
  
  CONCLUSIONS
  This review summarizes these recent studies with the goal of drawing conclusions about the activation or suppression of autophagy and mitophagy in the diabetic heart. A better understanding of how autophagy and mitophagy are affected in the diabetic myocardium is still needed, as well as whether they can be targeted therapeutically.
authors: Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, California.
authors: Dieter A
authors: DA
authors: Kubli
authors: Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, California.
authors: Åsa B
authors: ÅB
authors: Gustafsson
mesh_terms: D000818:Animals; D001343:Autophagy; D048909:Diabetes Complications / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000628:therapy; D003924:Diabetes Mellitus, Type 2 / Q000628:therapy; D058065:Diabetic Cardiomyopathies / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D006801:Humans; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism*