Edmarcia de Araujo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Edmarcia de Araujo has a total of 20 co-authors. Here are the top co-authors by number of shared publications:
- Andrea Baragetti
Department of Pharmacological Sciences “Rodolfo Paoletti”, University of Milan, Milan, Italy
1 shared publication Antonios Kourliouros
John Radcliffe Hospital, Oxford University Hospitals, United Kingdom (G.K, R.S., V.S., A.K., N.W., P.S.).
1 shared publication- Charalambos Antoniades
Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom
1 shared publication Cheng Xie
Division of Cardiovascular Medicine, Radcliffe Department of Medicine (M.D.P., I.B., J.C., C.X., E.W., I.A., D.F., P.P., E.d.A., C.P.K., K.M.C., C.A.), University of Oxford, United Kingdom
1 shared publicationChristos P. Kotanidis
Division of Cardiovascular Medicine, Radcliffe Department of Medicine (M.D.P., I.B., J.C., C.X., E.W., I.A., D.F., P.P., E.d.A., C.P.K., K.M.C., C.A.), University of Oxford, United Kingdom
1 shared publicationDaniel Foran
Division of Cardiovascular Medicine, Radcliffe Department of Medicine (M.D.P., I.B., J.C., C.X., E.W., I.A., D.F., P.P., E.d.A., C.P.K., K.M.C., C.A.), University of Oxford, United Kingdom
1 shared publication
Latest Publications
- Open Access
- 1 January 2026
- Published by Wolters Kluwer Health in Arteriosclerosis, Thrombosis, and Vascular Biology
- Vol. 46 (1) , 232-247
Lipoprotein(a) and Vascular Redox State in Patients With Advanced Coronary Atherosclerosis
BACKGROUND: Lp(a) (lipoprotein[a]) is associated with cardiovascular disease, but neither the causal nature nor the underlying mechanisms are fully documented. This study investigated whether Lp(a) triggers atherogenesis by dysregulating vascular redox–sensitive inflammatory state. METHODS: Plasma Lp(a) was measured in 1027 patients with advanced coronary artery disease undergoing cardiac surgery. These patients were genotyped, and a modified LPA genetic risk score (LPA GRS) determining Lp(a) levels was generated. RNA sequencing and vascular superoxide measurements were performed in internal mammary arteries, and the contribution of NOXs (NADPH oxidases) and uncoupled eNOS (endothelial nitric oxide synthase) was determined. The median follow-up was 5.07 years. RESULTS: Increased plasma Lp(a) ( P =0.03) and LPA GRS ( P =0.01) were associated with elevated arterial superoxide in the overall patient population, an effect that was driven by nondiabetics. This effect was primarily due to eNOS uncoupling via reduced vascular BH4 (tetrahydrobiopterin) bioavailability. There was no significant impact of Lp(a) variability on vascular NOX–derived superoxide ( P =0.13). RNA sequencing of arterial tissue revealed dysregulation of nitrosative and inflammatory signaling in high Lp(a) patients although there was no association with systemic biomarkers of inflammation (ie, hsCRP [high-sensitivity C-reactive protein]; P =0.82) or oxidative stress (ie, malondialdehyde; P =0.61). Finally, both LPA GRS (hazard ratio, 3.615 [95% CI, 1.044–12.515]; P =0.043) and high plasma Lp(a) (hazard ratio, 3.286 [95% CI, 1.003–10.767]; P =0.049) were associated with elevated risk for cardiac mortality. This association was vascular superoxide-dependent, implying that redox-sensitive inflammatory signaling may be a link between Lp(a) and cardiovascular risk. All the above associations were independent of plasma ApoB (apolipoprotein-B). CONCLUSIONS: This study demonstrates for the first time that a genetically determined increase in plasma Lp(a) results in dysregulated vascular redox/nitrosative signaling in patients with atherosclerosis.
- 1 January 2026
- Published by Wolters Kluwer Health in Arteriosclerosis, Thrombosis, and Vascular Biology
- Vol. 46 (1) , 232-247
Open AccessLipoprotein(a) and Vascular Redox State in Patients With Advanced Coronary Atherosclerosis
BACKGROUND: Lp(a) (lipoprotein[a]) is associated with cardiovascular disease, but neither the causal nature nor the underlying mechanisms are fully documented. This study investigated whether Lp(a) triggers atherogenesis by dysregulating vascular redox–sensitive inflammatory state. METHODS: Plasma Lp(a) was measured in 1027 patients with advanced coronary artery disease undergoing cardiac surgery. These patients were genotyped, and a modified LPA genetic risk score (LPA GRS) determining Lp(a) levels was generated. RNA sequencing and vascular superoxide measurements were performed in internal mammary arteries, and the contribution of NOXs (NADPH oxidases) and uncoupled eNOS (endothelial nitric oxide synthase) was determined. The median follow-up was 5.07 years. RESULTS: Increased plasma Lp(a) ( P =0.03) and LPA GRS ( P =0.01) were associated with elevated arterial superoxide in the overall patient population, an effect that was driven by nondiabetics. This effect was primarily due to eNOS uncoupling via reduced vascular BH4 (tetrahydrobiopterin) bioavailability. There was no significant impact of Lp(a) variability on vascular NOX–derived superoxide ( P =0.13). RNA sequencing of arterial tissue revealed dysregulation of nitrosative and inflammatory signaling in high Lp(a) patients although there was no association with systemic biomarkers of inflammation (ie, hsCRP [high-sensitivity C-reactive protein]; P =0.82) or oxidative stress (ie, malondialdehyde; P =0.61). Finally, both LPA GRS (hazard ratio, 3.615 [95% CI, 1.044–12.515]; P =0.043) and high plasma Lp(a) (hazard ratio, 3.286 [95% CI, 1.003–10.767]; P =0.049) were associated with elevated risk for cardiac mortality. This association was vascular superoxide-dependent, implying that redox-sensitive inflammatory signaling may be a link between Lp(a) and cardiovascular risk. All the above associations were independent of plasma ApoB (apolipoprotein-B). CONCLUSIONS: This study demonstrates for the first time that a genetically determined increase in plasma Lp(a) results in dysregulated vascular redox/nitrosative signaling in patients with atherosclerosis.