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1 Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia.
2 Laboratory of Cellular and Molecular Pathology of the Cardiovascular System, Avtsyn Research Institute of Human Morphology, Petrovsky National Research Centre of Surgery, Moscow, Russia.
3 Department of Biology and General Genetics, I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia.
4 The Cell Physiology and Pathology Laboratory, Orel State University Named After I.S.Turgenev, Orel, Russia.
5 Department of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Simrol, India.
6 Department of Microbiology, Immunology and Tropical Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, DC, United States.
7 Monzino Cardiology Center (IRCCS), Milan, Italy.
8 Diabetes Research Center, Beijing University of Chinese Medicine, Beijing, China.
9 Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow, Russia.
1 Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia.
2 Laboratory of Cellular and Molecular Pathology of the Cardiovascular System, Avtsyn Research Institute of Human Morphology, Petrovsky National Research Centre of Surgery, Moscow, Russia.
3 Department of Biology and General Genetics, I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia.
4 The Cell Physiology and Pathology Laboratory, Orel State University Named After I.S.Turgenev, Orel, Russia.
5 Department of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Simrol, India.
6 Department of Microbiology, Immunology and Tropical Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, DC, United States.
7 Monzino Cardiology Center (IRCCS), Milan, Italy.
8 Diabetes Research Center, Beijing University of Chinese Medicine, Beijing, China.
9 Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow, Russia.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Figures
Figure 1
Pathological factors contributing to the…
Figure 1
Pathological factors contributing to the development of atherosclerosis. Atherogenic LDL (desialylated, oxidized, and…
Figure 1
Pathological factors contributing to the development of atherosclerosis. Atherogenic LDL (desialylated, oxidized, and electronegative ones) induces lipid accumulation in endothelial cells and infiltrating macrophages, leading to foam cell formation, inflammation, and further progression of atherosclerosis. There are additional factors that contribute (or potentially contribute) to the development of atherogenesis, such as low levels of HDL, sialidase, and sialyl/galactosyltransferase activities leading to the generation of atherogenic LDL, intolerance to pro-inflammatory stimulation (including stimulation by atherogenic LDL), atherosclerosis-associated non-coding RNA (ncRNA), and exosomes.
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