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Pentraxin-3 and atherosclerosis risk: a Mendelian randomization study

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Abstract Objective: To assess the potential causal relationship between pentraxin 3 (PTX3) levels and atherosclerosis (AS) using a Mendelian randomization study. Methods: Data from genome-wide association studies (GWAS) were analyzed using the exposure factor PTX 3 and the outcome of atherosclerosis at different sites, including coronary atherosclerosis, peripheral atherosclerosis, cerebral atherosclerosis, and atherosclerosis at other sites (except cerebral, coronary, and peripheral arteries). The IVW method, MR⁃Egger method, WM method, method, and method were used for MR analysis, and heterogeneity tests, sensitivity analyses, and pleiotropy tests were performed. No artificial intelligence (AI) methods, such as large language models (LLMs), chatbots, or image creator-related assistive technologies, were used in this writing process. Results: Inverse variance weighting (IVW) analysis revealed no evidence of a causal association between PTX3 and the risk of coronary or peripheral atherosclerosis (OR=0.99, 95% CI=0.99-1.00, P=0.978; OR=1.01, 95% CI=0.92-1.11, P=0.723). No evidence of a causal association with the risk of cerebral atherosclerosis or other atherosclerosis was found (OR=1.18, 95% CI=0.7-2.01, P=0.524; OR=1.01, 95% CI=0.92-1.10, P=0.793). Conclusions There were no causal associations between PTX3 and coronary atherosclerosis, peripheral atherosclerosis, cerebral atherosclerosis, or atherosclerosis at other sites (except cerebral, coronary, or peripheral arteries).
Title: Pentraxin-3 and atherosclerosis risk: a Mendelian randomization study
Description:
Abstract Objective: To assess the potential causal relationship between pentraxin 3 (PTX3) levels and atherosclerosis (AS) using a Mendelian randomization study.
Methods: Data from genome-wide association studies (GWAS) were analyzed using the exposure factor PTX 3 and the outcome of atherosclerosis at different sites, including coronary atherosclerosis, peripheral atherosclerosis, cerebral atherosclerosis, and atherosclerosis at other sites (except cerebral, coronary, and peripheral arteries).
The IVW method, MR⁃Egger method, WM method, method, and method were used for MR analysis, and heterogeneity tests, sensitivity analyses, and pleiotropy tests were performed.
No artificial intelligence (AI) methods, such as large language models (LLMs), chatbots, or image creator-related assistive technologies, were used in this writing process.
Results: Inverse variance weighting (IVW) analysis revealed no evidence of a causal association between PTX3 and the risk of coronary or peripheral atherosclerosis (OR=0.
99, 95% CI=0.
99-1.
00, P=0.
978; OR=1.
01, 95% CI=0.
92-1.
11, P=0.
723).
No evidence of a causal association with the risk of cerebral atherosclerosis or other atherosclerosis was found (OR=1.
18, 95% CI=0.
7-2.
01, P=0.
524; OR=1.
01, 95% CI=0.
92-1.
10, P=0.
793).
Conclusions There were no causal associations between PTX3 and coronary atherosclerosis, peripheral atherosclerosis, cerebral atherosclerosis, or atherosclerosis at other sites (except cerebral, coronary, or peripheral arteries).

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