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Molecular Mechanisms of Atherosclerosis
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Molecular Mechanisms of Atherosclerosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 7517

Special Issue Editor

Dr. Michishige Terasaki

E-Mail Website
Guest Editor
Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-0064, Japan
Interests: macrophage; diabetic comorbidities; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dyslipidemia and diabetes increase the risk of atherosclerotic cardiovascular diseases, such as coronary artery disease, peripheral artery disease, and stroke. Various biochemical pathways activated under dyslipidemia and diabetic conditions can contribute to the acceleration of atherosclerosis. It is important to reveal the mechanisms of early characteristic features of atherosclerosis, which is considered to play a crucial role in the development and progression of atherosclerotic cardiovascular disease. For this Special Issue, we invite original research, review articles, rare case reports, and literature reviews on recent progress in molecular mechanisms of atherosclerosis in humans as well as animals.

Dr. Michishige Terasaki
Guest Editor

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Keywords

  • atherosclerosis
  • dyslipidemia
  • genes
  • macrophages
  • diabetes
  • molecular mechanisms

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Published Papers (4 papers)

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Research

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24 pages, 4757 KiB  
Article
An 8-SNP LDL Cholesterol Polygenic Score: Associations with Cardiovascular Risk Traits, Familial Hypercholesterolemia Phenotype, and Premature Coronary Heart Disease in Central Romania
by Ion Bogdan Mănescu, Manuela Rozalia Gabor, George Valeriu Moldovan, László Hadadi, Adina Huțanu, Claudia Bănescu and Minodora Dobreanu
Int. J. Mol. Sci. 2024, 25(18), 10038; https://doi.org/10.3390/ijms251810038 - 18 Sep 2024
Viewed by 863
Abstract
Familial hypercholesterolemia (FH) is the most significant inherited risk factor for coronary heart disease (CHD). Current guidelines focus on monogenic FH, but the polygenic form is more common and less understood. This study aimed to assess the clinical utility of an 8-SNP LDLC [...] Read more.
Familial hypercholesterolemia (FH) is the most significant inherited risk factor for coronary heart disease (CHD). Current guidelines focus on monogenic FH, but the polygenic form is more common and less understood. This study aimed to assess the clinical utility of an 8-SNP LDLC polygenic score in a central Romanian cohort. The cohort included 97 healthy controls and 125 patients with premature (P)CHD. The weighted LDLC polygenic risk score (wPRS) was analyzed for associations with relevant phenotypic traits, PCHD risk, and clinical FH diagnosis. The wPRS positively correlated with LDLC and DLCN scores, and LDLC concentrations could be predicted by wPRS. A trend of increasing LDLC and DLCN scores with wPRS deciles was observed. A +1 SD increase in wPRS was associated with a 36% higher likelihood of having LDLC > 190 mg/dL and increases in LDLC (+0.20 SD), DLCN score (+0.16 SD), and BMI (+0.15 SD), as well as a decrease in HDLC (−0.14 SD). Although wPRS did not predict PCHD across the entire spectrum of values, individuals above the 90th percentile were three times more likely to have PCHD compared to those within the 10th or 20th percentiles. Additionally, wPRS > 45th percentile identified “definite” clinical FH (DLCN score > 8) with 100% sensitivity and 45% specificity. The LDLC polygenic score correlates with key phenotypic traits, and individuals with high scores are more likely to have PCHD. Implementing this genetic tool may enhance risk prediction and patient stratification. These findings, the first of their kind in Romania, are consistent with the existing literature. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Atherosclerosis)
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Review

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27 pages, 2901 KiB  
Review
Current Strategies to Guide the Antiplatelet Therapy in Acute Coronary Syndromes
by Isabella Russo, Carola Griffith Brookles, Cristina Barale, Elena Melchionda, Amir Hassan Mousavi, Carloalberto Biolè, Alessandra Chinaglia and Matteo Bianco
Int. J. Mol. Sci. 2024, 25(7), 3981; https://doi.org/10.3390/ijms25073981 - 3 Apr 2024
Cited by 2 | Viewed by 2414
Abstract
The role of antiplatelet therapy in patients with acute coronary syndromes is a moving target with considerable novelty in the last few years. The pathophysiological basis of the treatment depends on platelet biology and physiology, and the interplay between these aspects and clinical [...] Read more.
The role of antiplatelet therapy in patients with acute coronary syndromes is a moving target with considerable novelty in the last few years. The pathophysiological basis of the treatment depends on platelet biology and physiology, and the interplay between these aspects and clinical practice must guide the physician in determining the best therapeutic options for patients with acute coronary syndromes. In the present narrative review, we discuss the latest novelties in the antiplatelet therapy of patients with acute coronary syndromes. We start with a description of platelet biology and the role of the main platelet signal pathways involved in platelet aggregation during an acute coronary syndrome. Then, we present the latest evidence on the evaluation of platelet function, focusing on the strengths and weaknesses of each platelet’s function test. We continue our review by describing the role of aspirin and P2Y12 inhibitors in the treatment of acute coronary syndromes, critically appraising the available evidence from clinical trials, and providing current international guidelines and recommendations. Finally, we describe alternative therapeutic regimens to standard dual antiplatelet therapy, in particular for patients at high bleeding risk. The aim of our review is to give a comprehensive representation of current data on antiplatelet therapy in patients with acute coronary syndromes that could be useful both for clinicians and basic science researchers to be up-to-date on this complex topic. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Atherosclerosis)
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16 pages, 1685 KiB  
Review
miRNA Regulation of Cell Phenotype and Parietal Remodeling in Atherosclerotic and Non-Atherosclerotic Aortic Aneurysms: Differences and Similarities
by Sonia Terriaca, Amedeo Ferlosio, Maria Giovanna Scioli, Francesca Coppa, Fabio Bertoldo, Calogera Pisano, Beatrice Belmonte, Carmela Rita Balistreri and Augusto Orlandi
Int. J. Mol. Sci. 2024, 25(5), 2641; https://doi.org/10.3390/ijms25052641 - 24 Feb 2024
Cited by 1 | Viewed by 1985
Abstract
Aortic aneurysms are a serious health concern as their rupture leads to high morbidity and mortality. Abdominal aortic aneurysms (AAAs) and thoracic aortic aneurysms (TAAs) exhibit differences and similarities in their pathophysiological and pathogenetic features. AAA is a multifactorial disease, mainly associated with [...] Read more.
Aortic aneurysms are a serious health concern as their rupture leads to high morbidity and mortality. Abdominal aortic aneurysms (AAAs) and thoracic aortic aneurysms (TAAs) exhibit differences and similarities in their pathophysiological and pathogenetic features. AAA is a multifactorial disease, mainly associated with atherosclerosis, characterized by a relevant inflammatory response and calcification. TAA is rarely associated with atherosclerosis and in some cases is associated with genetic mutations such as Marfan syndrome (MFS) and bicuspid aortic valve (BAV). MFS-related and non-genetic or sporadic TAA share aortic degeneration with endothelial-to-mesenchymal transition (End-Mt) and fibrosis, whereas in BAV TAA, aortic degeneration with calcification prevails. microRNA (miRNAs) contribute to the regulation of aneurysmatic aortic remodeling. miRNAs are a class of non-coding RNAs, which post-transcriptionally regulate gene expression. In this review, we report the involvement of deregulated miRNAs in the different aortic remodeling characterizing AAAs and TAAs. In AAA, miRNA deregulation appears to be involved in parietal inflammatory response, smooth muscle cell (SMC) apoptosis and aortic wall calcification. In sporadic and MFS-related TAA, miRNA deregulation promotes End-Mt, SMC myofibroblastic phenotypic switching and fibrosis with glycosaminoglycan accumulation. In BAV TAA, miRNA deregulation sustains aortic calcification. Those differences may support the development of more personalized therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Atherosclerosis)
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Other

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9 pages, 1522 KiB  
Case Report
A Clinical Case of Probable Sitosterolemia
by Michishige Terasaki, Mikiko Izumi and Sho-ichi Yamagishi
Int. J. Mol. Sci. 2024, 25(3), 1535; https://doi.org/10.3390/ijms25031535 - 26 Jan 2024
Viewed by 1601
Abstract
Sitosterolemia is a rare genetic lipid disorder characterized by elevated plant sterols in the serum. A 24-year-old Japanese woman was referred to our hospital due to a high serum low-density lipoprotein cholesterol (LDL-C) level of 332 mg/dL. At first, she was suspected to [...] Read more.
Sitosterolemia is a rare genetic lipid disorder characterized by elevated plant sterols in the serum. A 24-year-old Japanese woman was referred to our hospital due to a high serum low-density lipoprotein cholesterol (LDL-C) level of 332 mg/dL. At first, she was suspected to suffer from familial hypercholesterolemia, and thus received lipid-lowering agents. Although her LDL-C level remained high (220 mg/dL) with diet therapy plus 10 mg/day rosuvastatin, it was drastically decreased to 46 mg/dL with the addition of 10 mg/day ezetimibe. Finally, her LDL-C level was well-controlled at about 70 mg/dL with 10 mg/day ezetimibe alone. Furthermore, while her serum sitosterol level was elevated at 10.5 μg/mL during the first visit to our hospital, it decreased to 3.6 μg/mL with the 10 mg/day ezetimibe treatment alone. These observations suggest that she might probably suffer from sitosterolemia. Therefore, targeted gene sequencing analysis was performed using custom panels focusing on the exome regions of 21 lipid-associated genes, including ABCG5, ABCG8, and familial hypercholesterolemia-causing genes (LDL receptor, LDLRAP1, PCSK9, and apolipoprotein B). We finally identified a heterozygous ABCG8 variant (NM_022437.2:c.1285A>G or NP_071882.1:p.Met429Val) in our patient. The same gene mutation was detected in her mother. We report here a rare case exhibiting probable sitosterolemia caused by a heterozygous Met429Val variant in the ABCG8 gene and additional unknown variants. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Atherosclerosis)
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