Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Mar 28;92(11):609-15.
doi: 10.1016/j.lfs.2012.10.011. Epub 2012 Oct 30.

Diabetic cardiomyopathy and metabolic remodeling of the heart

Affiliations
Review

Diabetic cardiomyopathy and metabolic remodeling of the heart

Pavan K Battiprolu et al. Life Sci. .

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.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest

The authors have declared that no conflicts of interest exist.

Figures

Figure 1
Figure 1. New molecular targets and their role in diabetic cardiomyopathy
Schematic depiction of important elements of disease pathogenesis in diabetic cardiomyopathy, highlighting recently discovered molecular pathways.

References

    1. Gerstein HC, Miller ME, Genuth S, Ismail-Beigi F, Buse JB, Goff DC, Jr, Probstfield JL, Cushman WC, Ginsberg HN, Bigger JT, Grimm RH, Jr, Byington RP, Rosenberg YD, Friedewald WT ACCORD Study Group. Long-term effects of intensive glucose lowering on cardiovascular outcomes. N Engl J Med. 2011;364:818–28. - PMC - PubMed
    1. Back SH, Kaufman RJ. Endoplasmic Reticulum Stress and Type 2 Diabetes. Annu Rev Biochem. 2012 - PMC - PubMed
    1. Battiprolu PK, Gillette TG, Wang ZV, Lavandero S, Hill JA. Diabetic Cardiomyopathy: Mechanisms and Therapeutic Targets. Drug discovery today Disease mechanisms. 2010;7:e135–e43. - PMC - PubMed
    1. Battiprolu PK, Hojayev B, Jiang N, Wang ZV, Luo X, Iglewski M, et al. Metabolic stress-induced activation of FoxO1 triggers diabetic cardiomyopathy in mice. The Journal of clinical investigation. 2012;122:1109–18. - PMC - PubMed
    1. Borillo GA, Mason M, Quijada P, Volkers M, Cottage C, McGregor M, et al. Pim-1 kinase protects mitochondrial integrity in cardiomyocytes. Circ Res. 2010;106:1265–74. - PMC - PubMed

Publication types

MeSH terms