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Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition)

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A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2026) | Viewed by 22662

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Dr. Antonio Barbato

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Department of Clinical Medicine and Surgery, Federico II University of Naples Medical School, 80131 Naples, Italy
Interests: blood pressure; cardiovascular disease; metabolic syndrome; hypertension; atherosclerosis; cardiovascular epidemiology; metabolism; metabolic diseases; abdominal obesity; internal medicine
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Special Issue Information

Dear Colleagues,

Atherosclerosis is a common condition of vascular aging. However, several factors could influence this process, resulting in increased cardiovascular risk at a young age.

In addition to well-known factors (e.g., high blood pressure, dyslipidemia, diabetes, and excess body weight), there are several emerging factors associated with atherosclerosis, such as inflammation, endothelial dysfunction, intestinal microbiota alteration, uric acid, vitamin D, or miRNA expression, that could potentially explain the residual cardiovascular risk.

This Special Issue on atherosclerosis aims to report the most current scientific evidence available on this topic and reviews of the current literature on the role of emerging factors in the development of atherosclerosis, as demonstrated by both experimental and clinical studies, in order to gather a large body of data from which to start to highlight new potential objectives for reducing cardiovascular risk.

Dr. Antonio Barbato
Guest Editor

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Keywords

atherosclerosis
cardiovascular risk
arterial stiffness
blood pressure
vitamin D
miRNA
inflammation

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Published Papers (5 papers)

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Research

Jump to: Review

25 pages, 3598 KB

Open AccessArticle

Aortic Single-Cell Transcriptome Analysis Reveals ApoE-Isoform-Specific Influences on Vascular Disease

by David Y. Hui, Jeyashree Alagarsamy, April Haller, Mario Medvedovic and Anja Jaeschke

Int. J. Mol. Sci. 2026, 27(12), 5619; https://doi.org/10.3390/ijms27125619 - 22 Jun 2026

Viewed by 488

Abstract

The human APOE gene is polymorphic with three major alleles that encode apolipoprotein (apo) E2, apoE3, and apoE4. Both apoE2 and apoE4 are associated with increased atherosclerosis risk. This study utilized human APOE2, APOE3, and APOE4 gene replacement mice and single-cell RNA sequencing approach to delineate the mechanisms underlying this association. The human APOE2, APOE3, and APOE4 mice were fed a Western-type high fat–cholesterol diet for 16 weeks. Hyperlipidemia and significant atherosclerosis were observed in APOE2 mice but not in APOE3 or APOE4 mice. However, increased vascular inflammation was observed in both APOE2 and APOE4 mice. Single-cell RNA sequencing followed by cluster analysis identified 25 major cell types in the aorta that include various immune cell types, endothelial cells, and various vascular mural cell subsets. Results showed that cells from the APOE2 mice were enriched with genes associated with intracellular lipid accumulation and inflammation, whereas cells from the APOE4 mice displayed elevated oxidative- and/or endoplasmic reticulum-stress and inflammatory response. Thus, apoE2 accelerates atherosclerosis by inducing diet-induced hyperlipidemia and inflammation, while apoE4 does not induce hyperlipidemia but enhances inflammation that may prime the vasculature for atherosclerosis development. The distinct mechanisms by which apoE2 and apoE4 promote atherosclerosis underscore the importance of including apoE genotype information in the design of therapeutics for atherosclerosis intervention. Full article

(This article belongs to the Special Issue Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition))

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18 pages, 616 KB

Open AccessArticle

Noninvasive Assessment of Arterial Wall and Soluble ST2 in Patients with Type 2 Diabetes and Coronary Artery Disease

by Edyta Radzik, Marcin Schulz, Brygida Przywara-Chowaniec and Andrzej Tomasik

Int. J. Mol. Sci. 2025, 26(15), 7561; https://doi.org/10.3390/ijms26157561 - 5 Aug 2025

Cited by 1 | Viewed by 1299

Abstract

Diabetes-related pathophysiological processes contribute to endothelial dysfunction, arterial stiffening (AS), hypertension, vascular remodeling, and impaired myocardial perfusion. This study aimed to assess the relationship between arterial wall parameters and sST2 concentration as potential risk factors in type 2 diabetes (T2DM) and investigate sex-related differences. To achieve this, we enrolled 100 patients with suspected or exacerbated coronary artery disease (CAD) and divided them into a T2DM group (n = 58) and a control group (n = 42). Endothelial reactivity (lnRHI), ABI, sST2 levels, and carotid–femoral (cfPWV) and carotid–radial pulse wave velocity (crPWV) were assessed. Coronary angiography was performed in every patient, and epicardial flow and myocardial perfusion were evaluated using QuBE and FLASH. Our results showed that the coronary angiographic findings were similar in both groups. However, T2DM patients had a significantly higher central AS (cfPWV 10.8 ± 2 vs. 9.9 ± 2.7 m/s, p < 0.05) and vascular age (70.0 ± 12.3 vs. 61.3 ± 15.4 years, p < 0.05), while peripheral AS, RHI, and ABI showed no differences. CfPWV correlated with renal function; higher HbA1c and sST2 levels were additionally associated with advanced vascular age. Notably, central AS and vascular age were higher in men with T2DM but not in women. These findings indicate that T2DM patients exhibit increased central AS and vascular aging, influenced by sST2 levels, suggesting fibrosis as a target for precision medicine in T2DM. Full article

(This article belongs to the Special Issue Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition))

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Review

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29 pages, 1886 KB

Open AccessReview

Gut Microbiota and Atherosclerotic Plaque Instability: Cellular and Molecular Mechanisms

by Riccardo Nieri, Martina Pitolli, Matteo Antonio Russo and Federica Limana

Int. J. Mol. Sci. 2026, 27(13), 6001; https://doi.org/10.3390/ijms27136001 - 3 Jul 2026

Viewed by 581

Abstract

Atherosclerosis is a chronic multifactorial inflammatory vascular disease and the major risk factor for cardiovascular diseases (CVDs), characterized by arterial wall thickening, loss of arterial elasticity and the progressive accumulation of lipids and immune cells, ultimately leading to plaque formation and the development of unstable, rupture-prone plaques. Several studies suggest that gut microbiota might contribute to atherosclerosis, mainly by converting dietary and endogenous molecules into bioactive metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and the Gram-negative cell-wall component lipopolysaccharide (LPS). Such metabolites can promote key mechanisms involved in the development and progression of atherosclerotic plaque, and, importantly, plaque vulnerability. Specifically, they can worsen endothelial dysfunction, induce macrophage-driven inflammatory responses, and cause oxidative stress and extracellular matrix degradation. These processes are crucial for thinning of the fibrous cap and destabilization of atherosclerotic plaques. As a result, the risk of plaque rupture and related cardiovascular events increases. In this review, we summarize potential mechanisms by which the gut microbiota and their compounds induce the formation of vulnerable atherosclerotic plaques and discuss findings from experimental models and clinical studies that reveal the crucial role of microbiota–host dynamics in atherosclerosis. In contrast to previous reviews that primarily focused on atherosclerosis development, we specifically highlight the cellular and molecular mechanisms linking gut microbiota to plaque vulnerability and destabilization. We also address future research priorities to define microbiota-driven pathways better and develop targeted therapeutic interventions to reduce plaque vulnerability and cardiovascular risk. Full article

(This article belongs to the Special Issue Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition))

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21 pages, 1060 KB

Open AccessReview

Dysfunction of Microcirculation in Atherosclerosis: Implications of Nitric Oxide, Oxidative Stress, and Inflammation

by Marta Aleksandrowicz, Marek Konop, Mateusz Rybka, Łukasz Mazurek, Monika Stradczuk-Mazurek, Mateusz Kciuk, Bożena Bądzyńska, Leszek Dobrowolski and Marta Kuczeriszka

Int. J. Mol. Sci. 2025, 26(13), 6467; https://doi.org/10.3390/ijms26136467 - 4 Jul 2025

Cited by 23 | Viewed by 4740

Abstract

Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and most of them are connected with atherosclerosis (AS). Hypertension (HT), hyperlipidemia (HPL), and hyperglycaemia (HG) are the main risk factors responsible for CVD and have become a significant public health issue. AS might be a prime causative factor in CVD, and it originates from endothelial cell dysfunction. On the other hand, the factors mentioned above might cause endothelial cell damage as a consequence of endothelial dysfunction (ED) or might be regarded as a consequence of ED. Thus, endothelial cells are critical for maintaining vascular health and homeostasis, and their function is a key contributor to the initiation and progression of AS. The autoregulation of microcirculation, which is functionally present in the brain and kidneys, and from the physiological and pathophysiological point of view, is of high importance to preserve the proper function of the endothelium of blood vessels. The key factor responsible for cardiovascular system regulation and proper action is nitric oxide (NO). Disturbances in NO synthesis and/or bioavailability, caused by oxidative stress and/or inflammation, accompany or even precede diseases such as HT, angiogenesis-associated disorders, HPL, and HG, which are on the pathway of AS development. In the present review, we attempted to synthesize recent advances in understanding the pathophysiology of multifactorial-related AS. Full article

(This article belongs to the Special Issue Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition))

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26 pages, 1608 KB

Open AccessReview

Diabetes-Driven Atherosclerosis: Updated Mechanistic Insights and Novel Therapeutic Strategies

by Paschalis Karakasis, Panagiotis Theofilis, Dimitrios Patoulias, Panayotis K. Vlachakis, Antonios P. Antoniadis and Nikolaos Fragakis

Int. J. Mol. Sci. 2025, 26(5), 2196; https://doi.org/10.3390/ijms26052196 - 28 Feb 2025

Cited by 49 | Viewed by 14393

Abstract

The global rise in diabetes prevalence has significantly contributed to the increasing burden of atherosclerotic cardiovascular disease (ASCVD), a leading cause of morbidity and mortality in this population. Diabetes accelerates atherosclerosis through mechanisms such as hyperglycemia, oxidative stress, chronic inflammation, and epigenetic dysregulation, leading to unstable plaques and an elevated risk of cardiovascular events. Despite advancements in controlling traditional risk factors like dyslipidemia and hypertension, a considerable residual cardiovascular risk persists, highlighting the need for innovative therapeutic approaches. Emerging treatments, including sodium–glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, epigenetic modulators, and RNA-based therapies, are showing promise in addressing the unique challenges of diabetes-associated ASCVD. Precision medicine strategies, such as nanoparticle-based drug delivery and cell-specific therapies, offer further potential for mitigating cardiovascular complications. Advances in multiomics and systems biology continue to deepen our understanding of the molecular mechanisms driving diabetes-associated atherosclerosis. This review synthesizes recent advances in understanding the pathophysiology and treatment of diabetes-related atherosclerosis, offering a roadmap for future research and precision medicine approaches to mitigate cardiovascular risk in this growing population. Full article

(This article belongs to the Special Issue Atherosclerosis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (3rd Edition))

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