| A model on the induction of adverse vascular long-term effects of NSAIDs. | |
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MedLine Citation:
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PMID: 19149647 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The causes of increased rates of myocardial infarctions and strokes by application of non-steroidal anti-inflammatory agents (NSAIDs) are unclear. Here we present a biochemical model that the long-term vascular effects of NSAIDs can be consequences of their antiproliferative cellular mechanism. The analysis of the model suggests that the intramitochondrial uncoupling of oxidative phosphorylation induced by NSAIDs increases, through a reduced activity of ATP-dependent ionic pumps, the intra-cellular calcium x phosphate product with a consecutively increased formation and export of various calcium phosphate compounds. The latter cause, by chemical replication mechanisms of arterial hydroxyapatite deposits, a metatstatic calcifying vascular process. This sclerogenic vascular mineralization corresponds to an early arteriosclerotic development resembling the Mönckeberg's media calcification. The mechanism shows direct analogies to the accelerated and metastatic calcification of coronary arteries seen in chronic kidney disease and dialysis. This appears an extra-cellular time-lapse version of the protracted cell model. The induction of this degenerative mechanism may explain the increased number of adverse cardiovascular, renovascular and cerebrovascular effects of NSAIDs as they are observed in long-term therapies. |
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Authors:
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Rainer K Liedtke |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Medicinal chemistry (Shāriqah (United Arab Emirates)) Volume: 5 ISSN: 1573-4064 ISO Abbreviation: Med Chem Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2009-01-19 Completed Date: 2009-03-23 Revised Date: 2013-04-05 |
Medline Journal Info:
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Nlm Unique ID: 101240303 Medline TA: Med Chem Country: Netherlands |
Other Details:
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Languages: eng Pagination: 23-8 Citation Subset: IM |
Affiliation:
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Pharmed Institute of Cybernetics, Munich, Germany. liedtke@pharmed.de |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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antagonists & inhibitors,
metabolism Anti-Inflammatory Agents, Non-Steroidal / adverse effects* Calcinosis / chemically induced Calcium Phosphates / metabolism Cell Proliferation / drug effects Coronary Vessels / drug effects*, pathology*, physiopathology Humans Ion Channels / drug effects, metabolism Mitochondria / drug effects, metabolism Models, Biological* Myocardial Infarction / chemically induced Oxidative Phosphorylation / drug effects Stroke / chemically induced |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents, Non-Steroidal; 0/Calcium Phosphates; 0/Ion Channels; 56-65-5/Adenosine Triphosphate; 97Z1WI3NDX/calcium phosphate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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