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10/29/2014 7:34:00 PM | Browse: 520 | Download: 587
Publication Name World Journal of Gastroenterology
Manuscript ID 6631
Country of Manuscript Source Japan
Received
2013-10-31 17:08
Peer-Review Started
2013-11-14 22:22
To Make the First Decision
2014-01-09 12:38
Return for Revision
2014-03-06 12:12
Revised
2014-03-18 16:43
Second Decision
2014-06-13 15:54
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-06-13 16:22
Articles in Press
2014-06-13 16:24
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
2014-10-15 20:37
Publish the Manuscript Online
2014-10-29 19:34
ISSN 1007-9327 (print) and 2219-2840 (online)
Open Access
Copyright
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
Specialty Gastroenterology and Hepatology
Manuscript Type Topic Highlights
Article Title Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver
Manuscript Source Invited Manuscript
All Author List Jinyao Liu
Funding Agency and Grant Number
Corresponding author Jinyao Liu, MD, PhD, Department of Legal Medicine, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan. czhliu@yamaguchi-u.ac.jp
Keywords Alcohol; Fatty liver; Tumor necrosis factor-a; Hepatic stellate cell; Bone marrow-derived cell; Alcoholic liver disease
Core Tip Alcohol induces fatty liver by increasing the nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide ratio; increasing the activity of sterol regulatory element-binding protein (SREBP)-1, plasminogen activator inhibitor (PAI)-1, and early growth response-1; and decreasing peroxisome proliferator-activated receptor-? activity in liver. Alcohol activates the innate immune system and induces an imbalance in the immune response followed by the activation of Kupffer cell-derived tumor necrosis factor (TNF)-? overproduction, which is responsible for the dysregulated SREBP-1 and PAI-1 activity. Bone marrow-derived cells and sympathetic hyperactivity-activated hepatic stellate cells are also responsible for TNF-a overproduction in ethanol-induced hepatosteatosis. Carvedilol may attenuate the progression of ethanol-induced hepatosteatosis by suppressing sympathetic activity.
Publish Date 2014-10-29 19:34
Citation Liu J. Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver. World J Gastroenterol 2014; 20(40): 14672-14685
Url http://www.wjgnet.com/1007-9327/full/v20/i40/14672.htm
DOI http://dx.doi.org/10.3748/wjg.v20.i40.14672
Full Article (PDF) WJG-20-14672.pdf
Full Article (Word) WJG-20-14672.doc
Manuscript File 6631-Review.docx
Answering Reviewers 6631-Answering reviewers.pdf
Copyright License Agreement 6631-Copyright assignment.pdf
Non-Native Speakers of English Editing Certificate 6631-Language certificate.pdf
Peer-review Report 6631-Peer review(s).pdf
Scientific Misconduct Check 6631-CrossCheck.jpg
Scientific Editor Work List 6631-Scientific editor work list.pdf