TY  - JOUR
AU  - Vekić, Jelena
AU  - Stromsnes, Kristine
AU  - Mazzalai, Stefania
AU  - Zeljković, Aleksandra
AU  - Rizzo, Manfredi
AU  - Gambini, Juan
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5340
AB  - Oxidative stress is the consequence of an overproduction of reactive oxygen species (ROS) that exceeds the antioxidant defense mechanisms. Increased levels of ROS contribute to the development of cardiovascular disorders through oxidative damage to macromolecules, particularly by oxidation of plasma lipoproteins. One of the most prominent features of atherogenic dyslipidemia is plasma accumulation of small dense LDL (sdLDL) particles, characterized by an increased susceptibility to oxidation. Indeed, a considerable and diverse body of evidence from animal models and epidemiological studies was generated supporting oxidative modification of sdLDL particles as the earliest event in atherogenesis. Lipid peroxidation of LDL particles results in the formation of various bioactive species that contribute to the atherosclerotic process through different pathophysiological mechanisms, including foam cell formation, direct detrimental effects, and receptor-mediated activation of pro-inflammatory signaling pathways. In this paper, we will discuss recent data on the pathophysiological role of oxidative stress and atherogenic dyslipidemia and their interplay in the development of atherosclerosis. In addition, a special focus will be placed on the clinical applicability of novel, promising biomarkers of these processes.
PB  - MDPI
T2  - Biomedicines
T1  - Oxidative Stress, Atherogenic Dyslipidemia, and Cardiovascular Risk
VL  - 11
IS  - 11
DO  - 10.3390/biomedicines11112897
ER  - 

@article{
author = "Vekić, Jelena and Stromsnes, Kristine and Mazzalai, Stefania and Zeljković, Aleksandra and Rizzo, Manfredi and Gambini, Juan",
year = "2023",
abstract = "Oxidative stress is the consequence of an overproduction of reactive oxygen species (ROS) that exceeds the antioxidant defense mechanisms. Increased levels of ROS contribute to the development of cardiovascular disorders through oxidative damage to macromolecules, particularly by oxidation of plasma lipoproteins. One of the most prominent features of atherogenic dyslipidemia is plasma accumulation of small dense LDL (sdLDL) particles, characterized by an increased susceptibility to oxidation. Indeed, a considerable and diverse body of evidence from animal models and epidemiological studies was generated supporting oxidative modification of sdLDL particles as the earliest event in atherogenesis. Lipid peroxidation of LDL particles results in the formation of various bioactive species that contribute to the atherosclerotic process through different pathophysiological mechanisms, including foam cell formation, direct detrimental effects, and receptor-mediated activation of pro-inflammatory signaling pathways. In this paper, we will discuss recent data on the pathophysiological role of oxidative stress and atherogenic dyslipidemia and their interplay in the development of atherosclerosis. In addition, a special focus will be placed on the clinical applicability of novel, promising biomarkers of these processes.",
publisher = "MDPI",
journal = "Biomedicines",
title = "Oxidative Stress, Atherogenic Dyslipidemia, and Cardiovascular Risk",
volume = "11",
number = "11",
doi = "10.3390/biomedicines11112897"
}

Vekić, J., Stromsnes, K., Mazzalai, S., Zeljković, A., Rizzo, M.,& Gambini, J.. (2023). Oxidative Stress, Atherogenic Dyslipidemia, and Cardiovascular Risk. in Biomedicines
MDPI., 11(11).
https://doi.org/10.3390/biomedicines11112897

Vekić J, Stromsnes K, Mazzalai S, Zeljković A, Rizzo M, Gambini J. Oxidative Stress, Atherogenic Dyslipidemia, and Cardiovascular Risk. in Biomedicines. 2023;11(11).
doi:10.3390/biomedicines11112897 .

Vekić, Jelena, Stromsnes, Kristine, Mazzalai, Stefania, Zeljković, Aleksandra, Rizzo, Manfredi, Gambini, Juan, "Oxidative Stress, Atherogenic Dyslipidemia, and Cardiovascular Risk" in Biomedicines, 11, no. 11 (2023),
https://doi.org/10.3390/biomedicines11112897 . .