| Autor: |
Mushenkova NV; Pharmstandard Ventures, 10 Testovskaya Street, 123112 Moscow, Russia., Bezsonov EE; Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.; Institute of Human Morphology, 117418 Moscow, Russia., Orekhova VA; Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia., Popkova TV; V.A. Nasonova Institute of Rheumatology, 115522 Moscow, Russia., Starodubova AV; Federal Research Centre for Nutrition, Biotechnology and Food Safety, 109240 Moscow, Russia.; Therapy Faculty, Pirogov Russian National Research Medical University, 117997 Moscow, Russia., Orekhov AN; Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.; Institute of Human Morphology, 117418 Moscow, Russia. |
| Abstrakt: |
Atherosclerosis is a multifactorial chronic disease that has a prominent inflammatory component. Currently, atherosclerosis is regarded as an active autoimmune process that involves both innate and adaptive immune pathways. One of the drivers of this process is the presence of modified low-density lipoprotein (LDL). For instance, lipoprotein oxidation leads to the formation of oxidation-specific epitopes (OSE) that can be recognized by the immune cells. Macrophage response to OSEs is recognized as a key trigger for initiation and a stimulator of progression of the inflammatory process in the arteries. At the same time, the role of oxidized LDL components is not limited to pro-inflammatory stimulation, but includes immunoregulatory effects that can have protective functions. It is, therefore, important to better understand the complexity of oxidized LDL effects in atherosclerosis in order to develop new therapeutic approaches to correct the inflammatory and metabolic imbalance associated with this disorder. In this review, we discuss the process of oxidized LDL formation, mechanisms of OSE recognition by macrophages and the role of these processes in atherosclerosis. |
