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Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume...
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Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 7359

Special Issue Editor

Dr. Nikita G. Nikiforov

E-Mail Website
Guest Editor
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia
Interests: macrophage; monocyte; chronic inflammation; innate immunity; mitophagy; dysfunctional mitochondria; modified low density lipoprotein; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The modern inflammatory hypothesis of atherogenesis, which supplemented the classical cholesterol hypothesis, is now generally accepted and suggests the development of an effective therapy aimed at eliminating local chronic inflammation in the vessel wall. Thanks to Anichkov's cholesterol theory, it is well known that the accumulation of intracellular cholesterol in the vascular wall is a trigger for atherogenesis. However, not everything is so simple: approaches aimed at lowering blood cholesterol, LDL receptor regulation or cholesterol efflux showed insufficient effectiveness. However, they significantly improved the life expectancy and quality of life.

Recent advancements in new anti-inflammatory trials aiming to reduce cardiovascular complications only confirm the central role of chronic inflammation in CVD. Additionally, the importance of these trials can hardly be overestimated. The issue of uncovering the mechanisms underlying the chronification of the inflammatory response is now becoming especially urgent.

I think our current achievements are very similar to the success of physicists, hard at work on the Theory of Everything, which would explain the laws of the universe. Despite the complexity of our problem, I believe that humanity is already close to unraveling the underlying mechanisms of diseases, and we will be able to beat atherosclerosis, cancer, aging and, ultimately, death. However, we will then face completely different problems relating the economy, overpopulation and other aspects.

In this Special Issue, I want to collect the most recent publications on the mechanisms of the initiation of atherosclerosis and other age-related diseases. Studies on other important factors, such as lipid metabolism, genetic predisposition, the role of the microbiota, etc., as well as novel therapeutic approaches, are welcome. I also welcome research describing mitochondrial dysfunction, mtDNA mutations and the role of mitochondria in immune response.

Dr. Nikita G. Nikiforov
Guest Editor

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Keywords

  • atherosclerosis
  • cardiovascular diseases
  • molecular and cellular mechanisms
  • chronic inflammation
  • innate immunity
  • mitochondrial dysfunction
  • aging
  • inflammaging

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Published Papers (6 papers)

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Research

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10 pages, 652 KiB  
Article
Von Willebrand Factor Collagen-Binding Activity and Von Willebrand Factor-Mediated Platelet Adhesion in Patients with Coronary Artery Disease
by Zufar Gabbasov, Sergey Okhota, Yuliya Avtaeva, Olga Saburova, Ivan Melnikov, Valentina Shtelmakh, Sergey Bazanovich, Konstantin Guria and Sergey Kozlov
Biomedicines 2024, 12(9), 2007; https://doi.org/10.3390/biomedicines12092007 - 3 Sep 2024
Viewed by 454
Abstract
In this study, we investigated von Willebrand factor (VWF)-related parameters in 30 patients with stable coronary artery disease (CAD) and 50 patients without CAD. In both groups, the following were measured: the VWF antigen level (VWF:Ag); the VWF ristocetin cofactor activity (VWF:RCo); the [...] Read more.
In this study, we investigated von Willebrand factor (VWF)-related parameters in 30 patients with stable coronary artery disease (CAD) and 50 patients without CAD. In both groups, the following were measured: the VWF antigen level (VWF:Ag); the VWF ristocetin cofactor activity (VWF:RCo); the VWF collagen-binding activity (VWF:CB); and VWF-mediated platelet adhesion. Platelet adhesion was measured in whole blood at a shear rate of 1300 s−1 using a microfluidic chamber with a collagen-coated surface. VWF:Ag and VWF:RCo were found to be the same in both groups of patients. However, VWF:CB was found to be lower in patients with CAD compared with patients without CAD, with values of 106.7% (82.1; 131.6) and 160.4% (112.5; 218.1), respectively (p < 0.001). The decrease in platelet adhesion after GPIb inhibition was more pronounced in patients with CAD compared with patients of the control group, with recorded values of 76.0% (60.6; 82.1) and 29.3% (0.0; 60.4), respectively (p < 0.001). After adjusting for traditional risk factors, the odds ratio for CAD was found to be 0.98 (95% CI, 0.97–0.99; p = 0.011) per 1% increase in VWF:CB activity, and 1.06 (95% CI, 1.03–1.09; p < 0.001) per 1% decrease in GPIb-mediated platelet adhesion. The findings presented in this paper indicate a possible critical role played by complex VWF–collagen-platelet interactions in the development of CAD. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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17 pages, 508 KiB  
Article
Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis
by Margarita A. Sazonova, Tatiana V. Kirichenko, Anastasia I. Ryzhkova, Marina D. Sazonova, Natalya A. Doroschuk, Andrey V. Omelchenko, Nikita G. Nikiforov, Yulia I. Ragino and Anton Yu. Postnov
Biomedicines 2024, 12(8), 1868; https://doi.org/10.3390/biomedicines12081868 - 15 Aug 2024
Viewed by 673
Abstract
Background and Objectives: Atherosclerosis is one of the main reasons for cardiovascular disease development. This study aimed to analyze the association of mtDNA mutations and atherosclerotic plaques in carotid arteries of patients with atherosclerosis and conditionally healthy study participants from the Novosibirsk region. [...] Read more.
Background and Objectives: Atherosclerosis is one of the main reasons for cardiovascular disease development. This study aimed to analyze the association of mtDNA mutations and atherosclerotic plaques in carotid arteries of patients with atherosclerosis and conditionally healthy study participants from the Novosibirsk region. Methods: PCR fragments of DNA containing the regions of 10 investigated mtDNA mutations were pyrosequenced. The heteroplasmy levels of mtDNA mutations were analyzed using a quantitative method based on pyrosequencing technology developed by M. A. Sazonova and colleagues. Results: In the analysis of samples of patients with atherosclerotic plaques of the carotid arteries and conditionally healthy study participants from the Novosibirsk region, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected. A west–east gradient was found in the distribution of the mtDNA mutations m.5178C>A, m.3256C>T, m.652insG, and m.13513G>A. Conclusions: Therefore, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A, and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected in patients with atherosclerotic plaques in their carotid arteries from the Novosibirsk region. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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15 pages, 1024 KiB  
Article
The Blood Plasma Lipidomic Profile in Atherosclerosis of the Brachiocephalic Arteries
by Anastasiia Lomonosova, Daria Gognieva, Aleksandr Suvorov, Artemy Silantyev, Alina Abasheva, Yana Vasina, Magomed Abdullaev, Anna Nartova, Nikolay Eroshchenko, Viktoriia Kazakova, Roman Komarov, Andrey Dzyundzya, Elena Danilova, Dmitry Shchekochikhin and Philipp Kopylov
Biomedicines 2024, 12(6), 1279; https://doi.org/10.3390/biomedicines12061279 - 9 Jun 2024
Viewed by 1190
Abstract
According to the World Health Organization, ischemic stroke is the second leading cause of death in the world. Frequently, it is caused by brachiocephalic artery (BCA) atherosclerosis. Timely detection of atherosclerosis and its unstable course can allow for a timely response to potentially [...] Read more.
According to the World Health Organization, ischemic stroke is the second leading cause of death in the world. Frequently, it is caused by brachiocephalic artery (BCA) atherosclerosis. Timely detection of atherosclerosis and its unstable course can allow for a timely response to potentially dangerous changes and reduce the risk of vascular complications. Omics technologies allow us to identify new biomarkers that we can use in diagnosing diseases. This research included 90 blood plasma samples. The study group comprised 52 patients with severe atherosclerotic lesions BCA, and the control group comprised 38 patients with no BCA atherosclerosis. Targeted and panoramic lipidomic profiling of their blood plasma was carried out. There was a statistically significant difference (p < 0.05) in the values of the indices saturated fatty acids (FAs), unsaturated FAs, monounsaturated FAs, omega-3, and omega-6. Based on the results on the blood plasma lipidome, we formed models that have a fairly good ability to determine atherosclerotic lesions of the brachiocephalic arteries, as well as a model for identifying unstable atherosclerotic plaques. According only to the panoramic lipidome data, divided into groups according to stable and unstable atherosclerotic plaques, a significant difference was taken into account: p value < 0.05 and abs (fold change) > 2. Unfortunately, we did not observe significant differences according to the established plasma panoramic lipidome criteria between patients with stable and unstable plaques. Omics technologies allow us to obtain data about any changes in the body. According to our data, statistically significant differences in lipidomic profiling were obtained when comparing groups with or without BCA atherosclerosis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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19 pages, 7690 KiB  
Article
Atheroprotective Effect of Fucoidan in THP-1 Macrophages by Potential Upregulation of ABCA1
by Zeenat Mirza, Dalal A. Al-Saedi, Salma Saddeek, Sanaa Almowallad, Rehab F. AlMassabi and Etimad Huwait
Biomedicines 2023, 11(11), 2929; https://doi.org/10.3390/biomedicines11112929 - 30 Oct 2023
Cited by 5 | Viewed by 1511
Abstract
Targeting foam cells reduces the risk and pathophysiology of atherosclerosis, of which they are one of its early hallmarks. The precise mechanism of action of fucoidan, a potential anti-atherogenic drug, is still unknown. Our objective was to assess the ability of fucoidan to [...] Read more.
Targeting foam cells reduces the risk and pathophysiology of atherosclerosis, of which they are one of its early hallmarks. The precise mechanism of action of fucoidan, a potential anti-atherogenic drug, is still unknown. Our objective was to assess the ability of fucoidan to regulate expression of ATP-binding cassette transporter A1 (ABCA1) in ox-LDL-induced THP-1 macrophages. Molecular docking was used to predict how fucoidan interacts with anti-foam cell markers, and further in vitro experiments were performed to evaluate the protective effect of fucoidan on modulating uptake and efflux of lipids. THP-1 macrophages were protected by 50 µg/mL of fucoidan and were then induced to form foam cells with 25 µg/mL of ox-LDL. Expression levels were assessed using RT-qPCR, and an Oil Red O stain was used to observe lipid accumulation in THP-1 macrophages. In addition, ABCA1 protein was examined by Western blot, and cellular cholesterol efflux was determined using fluorescently labeled cholesterol. Under a light microscope, decreased lipid accumulation in ox-LDL-induced-THP-1 macrophages pre-treated with fucoidan showed a significant effect, although it did not affect the expression of scavenger receptors (SR-AI and CD36). It is interesting to note that fucoidan dramatically increased the gene and protein expression of ABCA1, perhaps via the liver X receptor-α (LXR-α). Moreover, fucoidan’s ability to increase and control the efflux of cholesterol from ox-LDL-induced THP-1 macrophages revealed how it may alter ABCA1’s conformation and have a major effect on how it interacts with apolipoprotein A (ApoA1). In vitro results support a rationale for predicting fucoidan and its interaction with its receptor targets’ predicted data, hence validating its anti-atherogenic properties and suggesting that fucoidan could be promising as an atheroprotective. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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Review

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13 pages, 889 KiB  
Review
T-Cell Metabolic Reprogramming in Atherosclerosis
by Shuye Chang, Zhaohui Wang and Tianhui An
Biomedicines 2024, 12(8), 1844; https://doi.org/10.3390/biomedicines12081844 - 14 Aug 2024
Viewed by 965
Abstract
Atherosclerosis is a key pathological basis for cardiovascular diseases, significantly influenced by T-cell-mediated immune responses. T-cells differentiate into various subtypes, such as pro-inflammatory Th1/Th17 and anti-inflammatory Th2/Treg cells. The imbalance between these subtypes is critical for the progression of atherosclerosis (AS). Recent studies [...] Read more.
Atherosclerosis is a key pathological basis for cardiovascular diseases, significantly influenced by T-cell-mediated immune responses. T-cells differentiate into various subtypes, such as pro-inflammatory Th1/Th17 and anti-inflammatory Th2/Treg cells. The imbalance between these subtypes is critical for the progression of atherosclerosis (AS). Recent studies indicate that metabolic reprogramming within various microenvironments can shift T-cell differentiation towards pro-inflammatory or anti-inflammatory phenotypes, thus influencing AS progression. This review examines the roles of pro-inflammatory and anti-inflammatory T-cells in atherosclerosis, focusing on how their metabolic reprogramming regulates AS progression and the associated molecular mechanisms of mTOR and AMPK signaling pathways. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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21 pages, 4406 KiB  
Review
Thymus in Cardiometabolic Impairments and Atherosclerosis: Not a Silent Player?
by Irina V. Kologrivova, Natalia V. Naryzhnaya and Tatiana E. Suslova
Biomedicines 2024, 12(7), 1408; https://doi.org/10.3390/biomedicines12071408 - 25 Jun 2024
Viewed by 1155
Abstract
The thymus represents a primary organ of the immune system, harboring the generation and maturation of T lymphocytes. Starting from childhood, the thymus undergoes involution, being replaced with adipose tissue, and by an advanced age nearly all the thymus parenchyma is represented by [...] Read more.
The thymus represents a primary organ of the immune system, harboring the generation and maturation of T lymphocytes. Starting from childhood, the thymus undergoes involution, being replaced with adipose tissue, and by an advanced age nearly all the thymus parenchyma is represented by adipocytes. This decline of thymic function is associated with compromised maturation and selection of T lymphocytes, which may directly impact the development of inflammation and induce various autoinflammatory disorders, including atherosclerosis. For a long time, thymus health in adults has been ignored. The process of adipogenesis in thymus and impact of thymic fat on cardiometabolism remains a mysterious process, with many issues being still unresolved. Meanwhile, thymus functional activity has a potential to be regulated, since islets of thymopoeisis remain in adults even at an advanced age. The present review describes the intricate process of thymic adipose involution, focusing on the issues of the thymus’ role in the development of atherosclerosis and metabolic health, tightly interconnected with the state of vessels. We also review the recent information on the key molecular pathways and biologically active substances that may be targeted to manipulate both thymic function and atherosclerosis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of CVD: Focus on Atherosclerosis (Volume II))
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