Publication Name	World Journal of Ophthalmology
Manuscript ID	12013
Country	Türkiye

Received	2014-06-17 15:10
Peer-Review Started	2014-06-18 17:22
To Make the First Decision	2014-07-29 11:52
Return for Revision	2014-08-07 08:40
Revised	2014-08-26 21:28
Second Decision	2014-09-17 13:59
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief	2014-09-17 14:26
Articles in Press	2014-09-17 14:26
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2014-11-04 16:40
Publish the Manuscript Online	2014-11-14 13:11

ISSN	2218-6239 (online)
Open Access
Copyright
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Website	http://www.wjgnet.com

Category	Ophthalmology
Manuscript Type	Minireviews
Article Title	Current evidence of pathophysiology of diabetic macular edema: A review
Manuscript Source	Invited Manuscript
All Author List	Gunhal Satirtav, Refik Oltulu and Hurkan Kerimoglu
Funding Agency and Grant Number
Corresponding Author	Gunhal Satirtav, MD, Ophthalmology Department, Necmettin Erbakan University Meram School of Medicine, Meram Tıp Fakultesi Hastanesi, Goz hastalıkları AD S-Blok 3. Kat, Meram, Konya 42800, Turkey. gunhal@gmail.com
Key Words	Diabetes mellitus; Macular edema; Pathophysiology; Vascular endothelial growth factor; Inflammation
Core Tip	Diabetic macular edema (DME) is an important cause of vision loss in patients with diabetes mellitus. The pathophysiology of DME can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the events that cause the edema to become chronic. On a macrocellular level, DME is believed to be in part caused by alterations in hydrostatic and oncotic pressures and shear stress. Angiogenic factor expression, inflammation and oxidative stress constitute the key components of microvascular pathways. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. Macular edema is thought to be caused as a result of these consequences.
Publish Date	2014-11-14 13:11
Citation	Satirtav G, Oltulu R, Kerimoglu H. Current evidence of pathophysiology of diabetic macular edema: A review. World J Ophthalmol 2014; 4(4): 147-151
URL	http://www.wjgnet.com/2218-6239/full/v4/i4/147.htm
DOI	http://dx.doi.org/10.5318/wjo.v4.i4.147

Full Article (PDF)	WJO-4-147.pdf
Full Article (Word)	WJO-4-147.doc
Manuscript File	12013-Review.doc
Answering Reviewers	12013-Answering reviewers.pdf
Copyright License Agreement	12013-Copyright assignment.pdf
Peer-review Report	12013-Peer review(s).pdf
Scientific Misconduct Check	12013-CrossCheck.jpg
Scientific Editor Work List	12013-Scientific editor work list.pdf