COX-2 Heart Risk Mechanism Suggested By Mouse Study Results
This article was originally published in The Tan Sheet
Executive Summary
Researchers may have identified the mechanism by which COX-2 inhibitors contribute to the risk of cardiovascular events, a study published in the April Journal of Clinical Investigation finds
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University of Pennsylvania researchers believe the findings of their new study suggest "the possibility of a new class of nonsteroidal anti-inflammatory drugs (NSAIDs) that steer clear of heart-disease risk and work to reduce it," according to a UPenn release. Deleting the inflammation enzyme microsomal (m)-PGE synthase (PGES)-1 gene in mice predisposed to hardening of the arteries had a "dramatic effect" on the development of atherosclerosis in male and female mice, Miao Wang, PhD, School of Medicine, UPenn, et al., found. Moreover, the deletion of mPGES-1 did not raise blood pressure or predispose the mice to thrombosis like COX-2 inhibition or deletion, the authors report in the Sept. 14 online edition of the Proceedings of the National Academy of Sciences. The PNAS study builds on a study published by the researchers earlier this year in the Journal of Clinical Investigation (1"The Tan Sheet" April 17, 2006, p. 8). The Journal of the American Medical Association released a study this week highlighting the cardiovascular risks associated with taking COX-2s...
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University of Pennsylvania researchers believe the findings of their new study suggest "the possibility of a new class of nonsteroidal anti-inflammatory drugs (NSAIDs) that steer clear of heart-disease risk and work to reduce it," according to a UPenn release. Deleting the inflammation enzyme microsomal (m)-PGE synthase (PGES)-1 gene in mice predisposed to hardening of the arteries had a "dramatic effect" on the development of atherosclerosis in male and female mice, Miao Wang, PhD, School of Medicine, UPenn, et al., found. Moreover, the deletion of mPGES-1 did not raise blood pressure or predispose the mice to thrombosis like COX-2 inhibition or deletion, the authors report in the Sept. 14 online edition of the Proceedings of the National Academy of Sciences. The PNAS study builds on a study published by the researchers earlier this year in the Journal of Clinical Investigation (1"The Tan Sheet" April 17, 2006, p. 8). The Journal of the American Medical Association released a study this week highlighting the cardiovascular risks associated with taking COX-2s...
Heart-healthy NSAIDs?
University of Pennsylvania researchers believe the findings of their new study suggest "the possibility of a new class of nonsteroidal anti-inflammatory drugs (NSAIDs) that steer clear of heart-disease risk and work to reduce it," according to a UPenn release. Deleting the inflammation enzyme microsomal (m)-PGE synthase (PGES)-1 gene in mice predisposed to hardening of the arteries had a "dramatic effect" on the development of atherosclerosis in male and female mice, Miao Wang, PhD, School of Medicine, UPenn, et al., found. Moreover, the deletion of mPGES-1 did not raise blood pressure or predispose the mice to thrombosis like COX-2 inhibition or deletion, the authors report in the Sept. 14 online edition of the Proceedings of the National Academy of Sciences. The PNAS study builds on a study published by the researchers earlier this year in the Journal of Clinical Investigation (1"The Tan Sheet" April 17, 2006, p. 8). The Journal of the American Medical Association released a study this week highlighting the cardiovascular risks associated with taking COX-2s...