Role of 14-3-3 protein and oxidative stress in diabetic cardiomyopathy.

Full Abstract

Cardiovascular disease is a leading cause of death worldwide. Diabetes mellitus is a well-known and important risk factor for cardiovascular diseases. The occurrence of diabetic cardiomyopathy is independent of hypertension, coronary artery disease, or any other known cardiac diseases. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Diabetic cardiomyopathy is characterized by morphologic and structural changes in the myocardium and coronary vasculature mediated by the activation of various signaling pathways. Myocardial apoptosis, hypertrophy and fibrosis are the most frequently proposed mechanisms to explain cardiac changes in diabetic cardiomyopathy. Mammalian 14-3-3 proteins are dimeric phosphoserine-binding proteins that participate in signal transduction and regulate several aspects of cellular biochemistry. 14-3-3 protein regulates diabetic cardiomyopathy via multiple signaling pathways. This review focuses on emerging evidence suggesting that 14-3-3 protein plays a key role in the pathogenesis of the cardiovascular complications of diabetes, which underlie the development and progression of diabetic cardiomyopathy.

Author information

Author/s: Watanabe, Kenichi (K); Thandavarayan, R A (RA); Gurusamy, N (N); Zhang, S (S); Muslin, A J (AJ); Suzuki, K (K); Tachikawa, H (H); Kodama, M (M); Aizawa, Y (Y);

Affiliation: Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, 265-1 Higashijima, Akiha-ku, Niigata City, Japan. watanabe(-atsign-)nupals.ac.jp

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Acta physiologica Hungarica (Acta Physiol Hung), published in Hungary. (Language: eng)

Reference: 2009-Sep; vol 96 (issue 3) : pp 277-87

Dates: Created 2009/08/26; Completed 2009/10/06;

PMID: 19706371, status: MEDLINE (last retrieval date: 10/6/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

External Links for this article
(including full text providers, if available):

Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.

This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.