A Novel Hypothesis: Erythrocyte Senescence Plays A Key Role In The Atherosclerosis Development

A. Deykin, Y. Silaeva, E. Leonova

Research output

Abstract

Background and Aims: Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by chronic inflammation, high blood pressure, oxidative stress, and progressive loss of cell and organ function with aging. We propose a hypothesis that the development of atherosclerosis is based on oxidative stress of erythrocytes and their senescence.

Methods: Our hypothesis is based on several facts. At the first, it is known that cholesterol content is increased in membrane of senescent erythrocytes. The second, senescent erythrocytes lose their plasticity and ability of deformation, which affects the rheological blood properties, that can injure the vessel wall. The third, macrophages are involved in all stages of atherogenesis. They can undergo polarization by shifting between M1 and M2 functional phenotypes.

Results: It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization and macrophage polarization toward the pro-inflammatory M1 macrophage is a major promoter to atheroma formation. It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization. A failure of efferocytosis leads to a prolongation of chronic pathology in tissue. In addition, fat-laden macrophages contribute to plague progression by transforming into foam cells in response to excess lipid deposition in arteries. We postulate that the main source of lipid accumulation in foam cells are senescent erythrocytes.

Conclusions: It is necessary to concentrate on the study of the role of senescent erythrocytes in atherogenesis, and to test our hypothesis in animal models. This work is supported by a grant from the Russian Scientific Foundation №17-75-20249
Original languageEnglish
Pages (from-to)e240-e241
JournalAtherosclerosis
Volume287
Publication statusE-pub ahead of print - 5 Aug 2019

Fingerprint

Atherosclerosis
Erythrocytes
Macrophages
Foam Cells
Oxidative Stress
Eating
Lipids
Plague
Organized Financing
Erythrocyte Membrane
Atherosclerotic Plaques
Chronic Disease
Animal Models
Arteries
Fats
Cholesterol
Pathology
Hypertension
Inflammation
Phenotype

Cite this

Deykin, A. ; Silaeva, Y. ; Leonova, E. / A Novel Hypothesis: Erythrocyte Senescence Plays A Key Role In The Atherosclerosis Development. In: Atherosclerosis. 2019 ; Vol. 287. pp. e240-e241.
@article{9590633e7db24218961aef13bf1e2612,
title = "A Novel Hypothesis: Erythrocyte Senescence Plays A Key Role In The Atherosclerosis Development",
abstract = "Background and Aims: Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by chronic inflammation, high blood pressure, oxidative stress, and progressive loss of cell and organ function with aging. We propose a hypothesis that the development of atherosclerosis is based on oxidative stress of erythrocytes and their senescence.Methods: Our hypothesis is based on several facts. At the first, it is known that cholesterol content is increased in membrane of senescent erythrocytes. The second, senescent erythrocytes lose their plasticity and ability of deformation, which affects the rheological blood properties, that can injure the vessel wall. The third, macrophages are involved in all stages of atherogenesis. They can undergo polarization by shifting between M1 and M2 functional phenotypes.Results: It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization and macrophage polarization toward the pro-inflammatory M1 macrophage is a major promoter to atheroma formation. It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization. A failure of efferocytosis leads to a prolongation of chronic pathology in tissue. In addition, fat-laden macrophages contribute to plague progression by transforming into foam cells in response to excess lipid deposition in arteries. We postulate that the main source of lipid accumulation in foam cells are senescent erythrocytes.Conclusions: It is necessary to concentrate on the study of the role of senescent erythrocytes in atherogenesis, and to test our hypothesis in animal models. This work is supported by a grant from the Russian Scientific Foundation №17-75-20249",
author = "A. Deykin and Y. Silaeva and E. Leonova",
year = "2019",
month = "8",
day = "5",
language = "English",
volume = "287",
pages = "e240--e241",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier",

}

A Novel Hypothesis: Erythrocyte Senescence Plays A Key Role In The Atherosclerosis Development. / Deykin, A.; Silaeva, Y.; Leonova, E.

In: Atherosclerosis, Vol. 287, 05.08.2019, p. e240-e241.

Research output

TY - JOUR

T1 - A Novel Hypothesis: Erythrocyte Senescence Plays A Key Role In The Atherosclerosis Development

AU - Deykin, A.

AU - Silaeva, Y.

AU - Leonova, E.

PY - 2019/8/5

Y1 - 2019/8/5

N2 - Background and Aims: Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by chronic inflammation, high blood pressure, oxidative stress, and progressive loss of cell and organ function with aging. We propose a hypothesis that the development of atherosclerosis is based on oxidative stress of erythrocytes and their senescence.Methods: Our hypothesis is based on several facts. At the first, it is known that cholesterol content is increased in membrane of senescent erythrocytes. The second, senescent erythrocytes lose their plasticity and ability of deformation, which affects the rheological blood properties, that can injure the vessel wall. The third, macrophages are involved in all stages of atherogenesis. They can undergo polarization by shifting between M1 and M2 functional phenotypes.Results: It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization and macrophage polarization toward the pro-inflammatory M1 macrophage is a major promoter to atheroma formation. It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization. A failure of efferocytosis leads to a prolongation of chronic pathology in tissue. In addition, fat-laden macrophages contribute to plague progression by transforming into foam cells in response to excess lipid deposition in arteries. We postulate that the main source of lipid accumulation in foam cells are senescent erythrocytes.Conclusions: It is necessary to concentrate on the study of the role of senescent erythrocytes in atherogenesis, and to test our hypothesis in animal models. This work is supported by a grant from the Russian Scientific Foundation №17-75-20249

AB - Background and Aims: Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by chronic inflammation, high blood pressure, oxidative stress, and progressive loss of cell and organ function with aging. We propose a hypothesis that the development of atherosclerosis is based on oxidative stress of erythrocytes and their senescence.Methods: Our hypothesis is based on several facts. At the first, it is known that cholesterol content is increased in membrane of senescent erythrocytes. The second, senescent erythrocytes lose their plasticity and ability of deformation, which affects the rheological blood properties, that can injure the vessel wall. The third, macrophages are involved in all stages of atherogenesis. They can undergo polarization by shifting between M1 and M2 functional phenotypes.Results: It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization and macrophage polarization toward the pro-inflammatory M1 macrophage is a major promoter to atheroma formation. It is known that efferocytosis, or ingestion of apoptotic cells, is stimulated by M2 macrophage polarization. A failure of efferocytosis leads to a prolongation of chronic pathology in tissue. In addition, fat-laden macrophages contribute to plague progression by transforming into foam cells in response to excess lipid deposition in arteries. We postulate that the main source of lipid accumulation in foam cells are senescent erythrocytes.Conclusions: It is necessary to concentrate on the study of the role of senescent erythrocytes in atherogenesis, and to test our hypothesis in animal models. This work is supported by a grant from the Russian Scientific Foundation №17-75-20249

UR - https://www.atherosclerosis-journal.com/article/S0021-9150(19)31195-5/fulltext

M3 - Meeting Abstract

VL - 287

SP - e240-e241

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -