title: The mitochondria in diabetic heart failure: from pathogenesis to therapeutic promise.
abstract: CONCLUSIONS
  Diabetes is an important risk factor for the development of heart failure (HF). Given the increasing prevalence of diabetes in the population, strategies are needed to reduce the burden of HF in these patients.
  
  
  BACKGROUND
  Diabetes is associated with several pathologic findings in the heart including dysregulated metabolism, lipid accumulation, oxidative stress, and inflammation. Emerging evidence suggests that mitochondrial dysfunction may be a central mediator of these pathologic responses. The development of therapeutic approaches targeting mitochondrial biology holds promise for the management of HF in diabetic patients.
  
  
  RESULTS
  Despite significant data implicating mitochondrial pathology in diabetic cardiomyopathy, the optimal pharmacologic approach to improve mitochondrial function remains undefined.
  
  
  CONCLUSIONS
  Detailed mechanistic studies coupled with more robust clinical phenotyping will be necessary to develop novel approaches to improve cardiac function in diabetes. Moreover, understanding the interplay between diabetes and other cardiac stressors (hypertension, ischemia, and valvular disease) will be of the utmost importance for clinical translation of scientific discoveries made in this field.
authors.affiliation: 1Diabetic Cardiovascular Disease Center, Washington University School of Medicine, St. Louis, Missouri.|2Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.|3Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: Joel D
authors.initials: JD
authors.lastname: Schilling
mesh_terms: D000818:Animals; D048909:Diabetes Complications / Q000378:metabolism; D058065:Diabetic Cardiomyopathies / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism*