Biological basis for the cardiovascular consequences of COX-2 inhibition: therapeutic challenges and opportunities.

By T. Grosser, Susanne Fries, G. FitzGerald. Journal of Clinical Investigation, 2005

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How researchers see this paper

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Selective COX-1 inhibition: A therapeutic target to be reconsidered. (2010, background): “The use of coxibs in the humans allowed to unravel the protective role of COX-2 for the cardiovascular system, mostly through the generation of the prostacyclin [9].”
Activation of Platelet Function Through G Protein–Coupled Receptors (2006, background): “A shape change is the initial response of platelets to activators such as thrombin, ADP, or TxA2.”
Adverse effects of nonsteroidal antiinflammatory drugs: an update of gastrointestinal, cardiovascular and renal complications. (2014, neutral): “The NSAIDs induced electrolyte imbalance, coupled with NSAIDs inhibitory effect on the production of vasodilator prostacyclin (PGI 2 ) (185), results in increased blood pressure, hypertension and consequently, CV complications.”
Non-steroidal anti-inflammatory drugs (NSAIDs) and organ damage: A current perspective (2020, neutral): “tween PGI2 and TxA2, thereby increasing the risk of CVD [152,165].”