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12/13/2014 7:02:00 PM | Browse: 652 | Download: 931
Publication Name World Journal of Diabetes
Manuscript ID 13711
Country/Territory United States
2014-08-29 08:28
Peer-Review Started
2014-08-29 17:30
To Make the First Decision
2014-09-16 10:52
Return for Revision
2014-09-19 18:11
2014-09-23 06:24
Second Decision
2014-11-03 17:00
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-11-03 17:12
Articles in Press
2014-11-03 17:12
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
2014-11-27 18:53
Publish the Manuscript Online
2014-12-13 19:01
ISSN 1948-9358 (online)
Open Access
Article Reprints For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
Permissions For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
Publisher Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Website http://www.wjgnet.com
Category Cardiac and Cardiovascular Systems
Manuscript Type Minireviews
Article Title Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart
Manuscript Source Invited Manuscript
All Author List Jia Zhao, Rushil Randive and James A Stewart
Funding Agency and Grant Number
Funding Agency Grant Number
American Heart Association SDG5310006 (JAS)
American Heart Association BGIA4150122 (JAS)
Corresponding Author James A Stewart, PhD, Assistant Professor, Department of Biological Sciences, Mississippi State University, 220 Harned Hall, 295 Lee Boulevard, PO Box GY, Mississippi State, MS 39762, United States. jstewart@biology.msstate.edu
Key Words Type 2 diabetes mellitus; Cardiac fibrosis; Fibroblasts; Advanced glycation end product; Rap1a; Extracellular matrix
Core Tip Chronic hyperglycemia is a characteristic of diabetes and one of the major causal factors of diabetic complications. In type 2 diabetes mellitus, mechanical and biochemical stimuli activated profibrotic signaling cascades resulting in myocardial fibrosis, impaired cardiac performance, and ventricular stiffness. Glucose nonenzymatically reacts with extracellular matrix (ECM) proteins forming advanced glycation end products (AGEs). AGE-modified collagen increases matrix accumulation and stiffness by engaging the receptor for AGE (RAGE), the receptor for AGE. To date, our understanding of the AGE/RAGE cascade remains imprecise. This review discusses the AGE/RAGE signaling cascade and proposes an alternate role for Rap1a in diabetic cardiovascular ECM remodeling.
Publish Date 2014-12-13 19:01
Citation Zhao J, Randive R, Stewart JA. Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart. World J Diabetes 2014; 5(6): 860-867
URL http://www.wjgnet.com/1948-9358/full/v5/i6/860.htm
DOI http://dx.doi.org/10.4239/wjd.v5.i6.860
Full Article (PDF) WJD-5-860.pdf
Full Article (Word) WJD-5-860.doc
Manuscript File 13711-Review.docx
Answering Reviewers 13711-Answering reviewers.pdf
Copyright License Agreement 13711-Copyright assignment.pdf
Peer-review Report 13711-Peer review(s).pdf
Scientific Misconduct Check 13711-CrossCheck.jpg
Scientific Editor Work List 13711-Scientific editor work list.pdf