| Gastroduodenal mucosal defense. | |
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MedLine Citation:
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PMID: 20948371 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: We have summarized recent findings related to gastroduodenal mucosal defense as well as factors contributing to defensive failure, highlighting findings that illuminate new pathophysiological mechanisms. RECENT FINDINGS: Gastroduodenal bicarbonate secretion is mediated by prostaglandin E receptors and stimulated by the prostone lubiprostone. Toll-like receptor (TLR)4 signaling is protective against gastric injury. Intestinal alkaline phosphatase (IAP) is a chemosensor that regulates the duodenal mucosal surface pH. Lipopolysaccharide (LPS) increases gastric permeability; IAP secreted during fat digestion may detoxify colonic LPS. NADPH oxidase activity mediates ischemia/reperfusion-related gastric mucosal damage. Heat shock protein 70 (HSP70) protects the gastric mucosa through inhibition of apoptosis, proinflammatory cytokines, and cell adhesion molecules (CAMs). HSP90 may be a contributing factor in impaired adaptive cytoprotection. Proteinase-activated receptor-1 (PAR-1) is protective against Helicobacter-induced gastritis, mediated by the suppression of proinflammatory pathways. IKK β/NF-κB signaling decreases chronic Helicobacter-induced inflammation by inhibiting cellular apoptosis and necrosis. Activation of A2A adenosine receptors decreases inflammation and gastritis but leads to persistent Helicobacter pylori infection. SUMMARY: Enhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight into potential therapeutic targets, contributing towards the development of better tolerated and more effective therapies. |
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Authors:
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Arushi deFoneska; Jonathan D Kaunitz |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review |
Journal Detail:
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Title: Current opinion in gastroenterology Volume: 26 ISSN: 1531-7056 ISO Abbreviation: Curr. Opin. Gastroenterol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-15 Completed Date: 2011-01-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8506887 Medline TA: Curr Opin Gastroenterol Country: United States |
Other Details:
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Languages: eng Pagination: 604-10 Citation Subset: IM |
Affiliation:
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Greater Los Angeles Veteran Affairs Healthcare System, WLAVA Medical Center, Department of Medicine, UCLA School of Medicine, Los Angeles, California 90073, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alkaline Phosphatase
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physiology Amino Acids / physiology Animals Anti-Inflammatory Agents, Non-Steroidal / adverse effects Bicarbonates / metabolism Gastric Mucosa / drug effects, metabolism*, physiology Heat-Shock Proteins / metabolism, physiology Helicobacter Infections / physiopathology Helicobacter pylori Humans Hypoxia-Inducible Factor 1 / physiology Intestinal Mucosa / metabolism*, physiology Oxidative Stress Peptides / metabolism, physiology Phosphodiesterase Inhibitors / pharmacology Prostaglandins / metabolism, physiology Reperfusion Injury / physiopathology Toll-Like Receptors / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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P30 DK0413/DK/NIDDK NIH HHS; R01 DK54221/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Amino Acids; 0/Anti-Inflammatory Agents, Non-Steroidal; 0/Bicarbonates; 0/Heat-Shock Proteins; 0/Hypoxia-Inducible Factor 1; 0/Peptides; 0/Phosphodiesterase Inhibitors; 0/Prostaglandins; 0/Toll-Like Receptors; 146046-78-8/trefoil factor; EC 3.1.3.1/Alkaline Phosphatase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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