Pericytes in Atherosclerosis

Summerhill, Volha I; Orekhov, Alexander N.

doi:10.1007/978-3-030-16908-4_13

Cited by 19 publications

(11 citation statements)

References 106 publications

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“…VSMCs are responsible for the coordination of physiologic processes required for homeostasis, for example, regulation of vascular tone and blood pressure. Pericytes support blood vessel integrity and normal functioning of the endothelial lining, forming multiple connections with the ECs [86,87]. These cells form a three-dimensional network being connected to each other and to the ECs and represent a second line of defense against pathogens under the endothelial lining [88].…”

Section: Pericytes and Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Salnikova

Orekhova

Grechko

et al. 2021

IJMS

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Altered mitochondrial function is currently recognized as an important factor in atherosclerosis initiation and progression. Mitochondrial dysfunction can be caused by mitochondrial DNA (mtDNA) mutations, which can be inherited or spontaneously acquired in various organs and tissues, having more or less profound effects depending on the tissue energy status. Arterial wall cells are among the most vulnerable to mitochondrial dysfunction due to their barrier and metabolic functions. In atherosclerosis, mitochondria cause alteration of cellular metabolism and respiration and are known to produce excessive amounts of reactive oxygen species (ROS) resulting in oxidative stress. These processes are involved in vascular disease and chronic inflammation associated with atherosclerosis. Currently, the list of known mtDNA mutations associated with human pathologies is growing, and many of the identified mtDNA variants are being tested as disease markers. Alleviation of oxidative stress and inflammation appears to be promising for atherosclerosis treatment. In this review, we discuss the role of mitochondrial dysfunction in atherosclerosis development, focusing on the key cell types of the arterial wall involved in the pathological processes. Accumulation of mtDNA mutations in isolated arterial wall cells, such as endothelial cells, may contribute to the development of local inflammatory process that helps explaining the focal distribution of atherosclerotic plaques on the arterial wall surface. We also discuss antioxidant and anti-inflammatory approaches that can potentially reduce the impact of mitochondrial dysfunction.

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Section: Pericytes and Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Salnikova

Orekhova

Grechko

et al. 2021

IJMS

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“…This cellular network appears to serve as a second line of defense after the endothelial layer within the arterial wall [22]. The stellate-shaped, pericyte-like cells can execute phagocytic functions alongside with macrophages and can participate in the immune response by producing pro-inflammatory cytokines [23]. Moreover, they can develop a capacity for antigen processing and presentation, like dendritic cells [24,25].…”

Section: Cellular Mechanisms Of Atherogenesismentioning

confidence: 99%

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Orekhov

Nikiforov

Ivanova

et al. 2020

JCM

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Chronification of inflammation is the process that lies at the basis of several human diseases that make up to 80% of morbidity and mortality worldwide. It can also explain a great deal of processes related to aging. Atherosclerosis is an example of the most important chronic inflammatory pathology in terms of public health impact. Atherogenesis is based on the inflammatory response of the innate immunity arising locally or focally. The main trigger for this response appears to be modified low-density lipoprotein (LDL), although other factors may also play a role. With the quick resolution of inflammation, atherosclerotic changes in the arterial wall do not occur. However, a violation of the innate immunity response can lead to chronification of local inflammation and, as a result, to atherosclerotic lesion formation. In this review, we discuss possible mechanisms of the impaired immune response with a special focus on mitochondrial dysfunction. Some mitochondrial dysfunctions may be due to mutations in mitochondrial DNA. Several mitochondrial DNA mutations leading to defective mitophagy have been identified. The regulatory role of mitophagy in the immune response has been shown in recent studies. We suggest that defective mitophagy promoted by mutations in mitochondrial DNA can cause innate immunity disorders leading to chronification of inflammation.

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“…It was shown that all types of intimal samples contain smooth muscle cells containing smooth muscle α-actin (approximately 50% of total cell population), the cells of hematogenic origin (lymphocytes and macrophages, from 3% to 20% of total cell population), and pericyte-like cells (from 30% to 40% of total cell population). More, pericyte-like cells in unaffected and atherosclerotic aortic intima are characterized by lowered proportion of resting cells in initial lesions and fatty streaks, and the increased proportion of activated cells in lipofibrous and fibrous plaques [60]. One should also consider the fact of simultaneous expression of macrophage antigen by subendothelial smooth muscle cells [61].…”

Section: Discussionmentioning

confidence: 99%

Heteroplasmic Variants of Mitochondrial DNA in Atherosclerotic Lesions of Human Aortic Intima

et al. 2019

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Mitochondrial dysfunction and oxidative stress are likely involved in atherogenesis. Since the mitochondrial genome variation can alter functional activity of cells, it is necessary to assess the presence in atherosclerotic lesions of mitochondrial DNA (mtDNA) heteroplasmic mutations known to be associated with different pathological processes and ageing. In this study, mtDNA heteroplasmy and copy number (mtCN) were evaluated in the autopsy-derived samples of aortic intima differing by the type of atherosclerotic lesions. To detect mtDNA heteroplasmic variants, next generation sequencing was used, and mtCN measurement was performed by qPCR. It was shown that mtDNA heteroplasmic mutations are characteristic for particular areas of intimal tissue; in 83 intimal samples 55 heteroplasmic variants were found; mean minor allele frequencies level accounted for 0.09, with 12% mean heteroplasmy level. The mtCN variance measured in adjacent areas of intima was high, but atherosclerotic lesions and unaffected intima did not differ significantly in mtCN values. Basing on the ratio of minor and major nucleotide mtDNA variants, we can conclude that there exists the increase in the number of heteroplasmic mtDNA variants, which corresponds to the extent of atherosclerotic morphologic phenotype.

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Pericytes in Atherosclerosis

Cited by 19 publications

References 106 publications

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Heteroplasmic Variants of Mitochondrial DNA in Atherosclerotic Lesions of Human Aortic Intima

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