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March 6, 2001Proceedings of the National Academy of SciencesOpen Access

Acceleration of atherogenesis by COX-1-dependent prostanoid formation in low density lipoprotein receptor knockout mice

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Why the study?

Does selective COX-2 inhibition or non-selective COX inhibition alter the rate of atherogenesis in fat-fed low density lipoprotein receptor knockout mice?

Population

Fat-fed low density lipoprotein receptor knockout mice

Design

Preclinical

Authors

DPDomenico PraticòTemple UniversityTCTillmann CyrusWashington University in St. LouisZZZhibing ZhangTongji Hospital

Discussion

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Implication

Hypothesis-generating for COX-1 involvement in murine atherogenesis; leaves open any effect of COX inhibitors on human plaque progression.

Structured PICO

Does selective COX-2 inhibition or non-selective COX inhibition alter the rate of atherogenesis in fat-fed low density lipoprotein receptor knockout mice?

P
Population
Fat-fed low density lipoprotein receptor knockout mice
I
Intervention
Nimesulide (selective COX-2 inhibitor) or Indomethacin (isoform nonspecific COX inhibitor)
O
Outcome
Extent of atherosclerosissurrogate

In a mouse model, non-selective COX inhibition reduced atherosclerosis while selective COX-2 inhibition did not accelerate it, implicating COX-1-derived prostanoids in atherogenesis.

Cite This Study

Praticò et al. (2001) studied this question.

synapsesocial.com/papers/6a83b5ded65172829ee659b9https://doi.org/10.1073/pnas.061607398

Topics

Coronary artery disease
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  5. 5Coagulation defects and altered hemodynamic responses in mice lacking receptors for thromboxane A2.1998 · 276 citations