Abstract
Diabetic cardiomyopathy (DCM) is a disorder of the heart muscle in people with diabetes that can occur independent of hypertension or vascular disease. The underlying mechanism of DCM is incompletely understood. Some transcription factors have been suggested to regulate the gene program intricate in the pathogenesis of diabetes prompted cardiac injury. Forkhead box transcription factor 1 is a pleiotropic transcription factor that plays a pivotal role in a variety of physiological processes. Altered FOXO1 expression and function have been associated with cardiovascular diseases, and the important role of FOXO1 in DCM has begun to attract attention. In this review, we focus on the FOXO1 pathway and its role in various processes that have been related to DCM, such as metabolism, oxidative stress, endothelial dysfunction, inflammation and apoptosis.
Highlights
Diabetic cardiomyopathy (DCM) is causative for 80 % of the fatality rate in the diabetic inhabitants [1, 2]
forkhead box transcriptional factor (FOXO) regulation may deed in DCM via numerous pathways, by governing different set of genes being involved in allied processes such as oxidative stress, metabolism, inflammation, endothelial dysfunction and apoptosis
In summary, FOXO1 regulation may contribute to the detrimental outcomes of the cardiac cells in diabetes, accelerating the development of DCM, one of the predominant cardiac difficulties in diabetic patients
Summary
Diabetic cardiomyopathy (DCM) is causative for 80 % of the fatality rate in the diabetic inhabitants [1, 2]. FOXO regulation may deed in DCM via numerous pathways, by governing different set of genes being involved in allied processes such as oxidative stress, metabolism, inflammation, endothelial dysfunction and apoptosis. Within the setting of cardiac function, the FOXO proteins are supposed to be participated in oxidative stress [63], regulation of metabolism [58], cell cycle [64], and cell death [65].
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.