Diabetic cardiomyopathy and metabolic remodeling of the heart

Pavan K. Battiprolu, Camila Lopez-Crisosto, Zhao V. Wang, Andriy Nemchenko, Sergio Lavandero, Joseph A. Hill

Research output: Contribution to journalReview articlepeer-review

79 Citations (Scopus)

Abstract

The incidence and prevalence of diabetes mellitus are both increasing rapidly in societies around the globe. The majority of patients with diabetes succumb ultimately to heart disease, much of which stems from atherosclerotic disease and hypertension. However, the diabetic milieu is itself intrinsically noxious to the heart, and cardiomyopathy can develop independent of elevated blood pressure or coronary artery disease. This process, termed diabetic cardiomyopathy, is characterized by significant changes in the physiology, structure, and mechanical function of the heart. Presently, therapy for patients with diabetes focuses largely on glucose control, and attention to the heart commences with the onset of symptoms. When the latter develops, standard therapy for heart failure is applied. However, recent studies highlight that specific elements of the pathogenesis of diabetic heart disease are unique, raising the prospect of diabetes-specific therapeutic intervention. Here, we review recently unveiled insights into the pathogenesis of diabetic cardiomyopathy and associated metabolic remodeling with an eye toward identifying novel targets with therapeutic potential.

Original languageEnglish
Pages (from-to)609-615
Number of pages7
JournalLife Sciences
Volume92
Issue number11
DOIs
Publication statusPublished - 2013

Bibliographical note

Funding Information:
This work was supported by grants from the NIH ( HL-075173 , J.A.H.; HL-080144 , J.A.H.; HL-090842 , J.A.H.), AHA ( 0640084N , J.A.H.; 12POST9030041 , P.K.B.), ADA mentor-based postdoctoral fellowship ( 7-08-MN-21-ADA , J.A.H. and P.K.B.), the AHA-Jon Holden DeHaan Foundation ( 0970518N , J.A.H.), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico : FONDECYT 1120212 and ACT1111 (S.L.). C.L.C. is a recipient of a CONICYT fellowship , Chile.

Funding

This work was supported by grants from the NIH ( HL-075173 , J.A.H.; HL-080144 , J.A.H.; HL-090842 , J.A.H.), AHA ( 0640084N , J.A.H.; 12POST9030041 , P.K.B.), ADA mentor-based postdoctoral fellowship ( 7-08-MN-21-ADA , J.A.H. and P.K.B.), the AHA-Jon Holden DeHaan Foundation ( 0970518N , J.A.H.), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico : FONDECYT 1120212 and ACT1111 (S.L.). C.L.C. is a recipient of a CONICYT fellowship , Chile.

FundersFunder number
AHA-Jon Holden DeHaan Foundation0970518N
National Institutes of HealthHL-075173, HL-080144
National Heart, Lung, and Blood InstituteR01HL090842
American Heart Association12POST9030041, 0640084N
Comisión Nacional de Investigación Científica y Tecnológica
Fondo Nacional de Desarrollo Científico y Tecnológico1120212, ACT1111
Aeronautical Development Agency

    ASJC Scopus Subject Areas

    • General Pharmacology, Toxicology and Pharmaceutics
    • General Biochemistry,Genetics and Molecular Biology

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