Editorial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Mar 15, 2015; 6(2): 217-224
Published online Mar 15, 2015. doi: 10.4239/wjd.v6.i2.217
mTOR: Driving apoptosis and autophagy for neurocardiac complications of diabetes mellitus
Kenneth Maiese
Kenneth Maiese, Cellular and Molecular Signaling, Newark, NJ 07101, United States
Author contributions: Maiese K conceived, designed, and wrote this article.
Supported by The following grants to Kenneth Maiese: American Diabetes Association; American Heart Association; NIH NIEHS; NIH NIA; NIH NINDS; and NIH ARRA.
Conflict-of-interest: The author declares no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Kenneth Maiese, MD, Cellular and Molecular Signaling, Newark, NJ 07101, United States. wntin75@yahoo.com
Received: November 2, 2014
Peer-review started: November 2, 2014
First decision: November 27, 2014
Revised: December 10, 2014
Accepted: January 15, 2015
Article in press: January 19, 2015
Published online: March 15, 2015
Processing time: 137 Days and 16.8 Hours
Core Tip

Core tip: The pathways of mechanistic target of rapamycin (mTOR) linked to mTOR complex 1, mTOR complex 2, AMP activated protein kinase, and tuberous sclerosis 1/tuberous sclerosis 2 complex can offer novel strategies for the complications of diabetes mellitus to prevent death and disability for the millions of individuals afflicted with this disorder.