Document Detail

A model on the induction of adverse vascular long-term effects of NSAIDs.
MedLine Citation:
PMID:  19149647     Owner:  NLM     Status:  MEDLINE    
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.
Rainer K Liedtke
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Medicinal chemistry (Shāriqah (United Arab Emirates))     Volume:  5     ISSN:  1573-4064     ISO Abbreviation:  Med Chem     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-01-19     Completed Date:  2009-03-23     Revised Date:  2013-04-05    
Medline Journal Info:
Nlm Unique ID:  101240303     Medline TA:  Med Chem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  23-8     Citation Subset:  IM    
Pharmed Institute of Cybernetics, Munich, Germany.
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MeSH Terms
Adenosine Triphosphate / 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
Ion Channels / drug effects,  metabolism
Mitochondria / drug effects,  metabolism
Models, Biological*
Myocardial Infarction / chemically induced
Oxidative Phosphorylation / drug effects
Stroke / chemically induced
Reg. No./Substance:
0/Anti-Inflammatory Agents, Non-Steroidal; 0/Calcium Phosphates; 0/Ion Channels; 56-65-5/Adenosine Triphosphate; 97Z1WI3NDX/calcium phosphate

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