Special Issue "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 "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 January 2024 | Viewed by 678

Special Issue 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

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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

Published Papers (1 paper)

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19 pages, 7690 KiB  
Atheroprotective Effect of Fucoidan in THP-1 Macrophages by Potential Upregulation of ABCA1
Biomedicines 2023, 11(11), 2929; https://doi.org/10.3390/biomedicines11112929 - 30 Oct 2023
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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
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