SUMMARY |
ARTERIAL VASCULAR EFFECTS OF NSAIDS AS A BIOCHEMICAL MODEL FOR AN INDUCTION OF ARTERIOSCLEROSIS |
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| The anti-proliferative effects of non-steroidal anti-inflammatory drugs (NSAIDs) can serve as model for the induction and development of vascular calcification and arteriosclerosis. |
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| A calcification cascade. An NSAID induced reduction of mitochondrial ATP synthesis effects in the cell an accumulation of phosphates and calcium ions (1). This triggers a chemical formation of calcium phosphates (2) and a subsequent formation and deposition of hydroxylapatite complexes (HAP) (3). A process of a chemical self-assembly (CSA) produces further HAP. These are exported and induce a mineralizing process in the arterial medial layer. The calcified vessels effect on their part a reduced cell supply and increase the cell energy impairment (modified excerpt from: A model on the induction of adverse long-term effects of NSAIDs; Med Chem 2009, 5(1), 23) |
CONCLUSIONS |
- NSAIDs can induce an intracellular formation of calcifying compounds which effect arteriosclerotic processes. This is not a result of a COX-inhibition.
- The initial mineralizing process occurs in the arterial medial layer and suggests a development of an early hypertension. The calcifying processes show also an analogy to the metastatic cardiovascular complications in chronic kidney diseases, in particular in those with a hemodialysis.
- The arteriosclerotic calcification processes are subject to conditions of a chemical balance, therefore may be therapeutically influenceable.
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© 2010 Rainer K Liedtke |
