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Victoria A. Khotina

Researcher at Russian Academy

Publications -  21
Citations -  239

Victoria A. Khotina is an academic researcher from Russian Academy. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 4, co-authored 11 publications receiving 82 citations.

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Lipid Metabolism in Macrophages: Focus on Atherosclerosis.

TL;DR: This review summarizes the existing knowledge on the involvement of macrophage lipid metabolism in atherosclerosis development, including both the results of recent studies and classical concepts, and provides a detailed description of these processes from the moment of lipid uptake with lipoproteins to cholesterol efflux.
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Signaling Pathways and Key Genes Involved in Regulation of foam Cell Formation in Atherosclerosis.

TL;DR: It has been demonstrated that the formation of foam cells is induced by modified low-density lipoprotein (LDL), and the beneficial effects of the majority of therapeutic strategies with generalized action, such as the use of anti-inflammatory drugs or antioxidants, were not confirmed by clinical studies.
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NADPH Oxidases and Their Role in Atherosclerosis.

TL;DR: Despite the growing evidence of the crucial involvement of NADPH oxidases in atherosclerosis pathogenesis, the available data still remains controversial and the future directions of research are outlined.
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The Role of the VEGF Family in Atherosclerosis Development and Its Potential as Treatment Targets

TL;DR: Several modern anti-atherosclerosis VEGFs-targeted experimental procedures, drugs and natural compounds, which could significantly improve the efficiency of atherosclerosis and related CVDs’ treatment are discussed.
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Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response

TL;DR: The underlying mechanisms of ER stress formation and the interplay of lipid accumulation and pro-inflammatory response are discussed, which will specifically focus on macrophages, which are the key players in maintaining chronic inflammatory milieu in atherosclerotic lesions, and also a major source of lipid-accumulating foam cells.