Mañana, JUEVES, 24 DE ABRIL, el sistema se apagará debido a tareas habituales de mantenimiento a partir de las 9 de la mañana. Lamentamos las molestias.
Targeting metabolic disturbance in the diabetic heart
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)Publisher
BioMed CentralDate
2015-02-07Citation
10.1186/s12933-015-0173-8
Cardiovascular Diabetology 14.1 (2015): 17
ISSN
1475-2840DOI
10.1186/s12933-015-0173-8Funded by
This work was supported by national grants from Ministerio de Educación y Ciencia (SAF2009-08367) and Comunidad de Madrid (CCG10-UAM/BIO-5289).Project
Gobierno de España. SAF2009-08367; Comunidad de Madrid. CCG10-UAM/BIO-5289Editor's Version
http://dx.doi.org/10.1186/s12933-015-0173-8Subjects
Advanced glycation end-products; Diabetic cardiomyopathy; Metformin; Dipeptidyl peptidase-4; Statins; Peroxisome proliferator activated receptor agonists; Fatty acid translocase/cluster of differentiation-36; Toll-like receptor-4; Nod-like receptor-3; MedicinaRights
© 2015 Fuentes-Antrás et al.Abstract
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
Files in this item
Google Scholar:Fuentes-Antrás, Jesús
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Picatoste, Belén
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Ramírez, Elisa
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Egido, Jesús
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Tuñón Fernández, José Luis
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Lorenzo González, Óscar
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