Targeting metabolic disturbance in the diabetic heart

Cardiovascular Diabetology

Óscar Lorenzo²  José Tuñón¹  Jesús Egido²  Elisa Ramírez²  Belén Picatoste²  Jesús Fuentes-Antrás¹ 

[1] Vascular, Renal and Diabetes Laboratory, IIS-Fundación Jiménez Díaz, Autónoma University, Av. Reyes Católicos 2, Madrid 28040, Spain;Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM) network, Madrid, Spain

关键词: Nod-like receptor-3;    Toll-like receptor-4;    Fatty acid translocase/cluster of differentiation-36;    Peroxisome proliferator activated receptor agonists;    Statins;    Advanced glycation end-products;    Glucagon-like protein-1;    Dipeptidyl peptidase-4;    Metformin;    Diabetic cardiomyopathy;   

Others  :  1123409
DOI  :  10.1186/s12933-015-0173-8

 received in 2014-11-04, accepted in 2015-01-02,  发布年份 2015

【 摘 要 】

Diabetic cardiomyopathy is defined as ventricular dysfunction initiated by alterations in cardiac energy substrates in the absence of coronary artery disease and hypertension. In addition to the demonstrated burden of cardiovascular events associated with diabetes, diabetic cardiomyopathy partly explains why diabetic patients are subject to a greater risk of heart failure and a worse outcome after myocardial ischemia. The raising prevalence and accumulating costs of cardiovascular disease in diabetic patients underscore the deficiencies of tertiary prevention and call for a shift in medical treatment. It is becoming increasingly clearer that the effective prevention and treatment of diabetic cardiomyopathy require measures to regulate the metabolic derangement occurring in the heart rather than merely restoring suitable systemic parameters. Recent research has provided deeper insight into the metabolic etiology of diabetic cardiomyopathy and numerous heart-specific targets that may substitute or reinforce current strategies. From both experimental and translational perspectives, in this review we first discuss the progress made with conventional therapies, and then focus on the need for prospective metabolic targets that may avert myocardial vulnerability and functional decline in next-generation diabetic care.

【 授权许可】

   
2015 Fuentes-Antrás et al.; licensee BioMed Central.

【 图 表 】

Figure1.

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