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New Cardiovascular Risk Factors: 2nd Edition
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New Cardiovascular Risk Factors: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 May 2026 | Viewed by 10476

Special Issue Editor

Dr. Antonio Barbato

E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals

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, 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 focused on cardiovascular risk factors 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

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • atherosclerosis
  • cardiovascular risk
  • arterial stiffness
  • blood pressure
  • vitamin D
  • miRNA
  • inflammation

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Related Special Issue

Published Papers (4 papers)

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Research

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13 pages, 500 KB  
Article
Protective Effect of Factor XIII Intron-K G Allele on Subclinical Vascular Disease
by Barbara Cogoi, Regina Esze, Sándor Somodi, Amir H. Shemirani, Zsuzsanna Bereczky, László Muszbek, György Paragh, Mónika Katkó and Miklós Káplár
Int. J. Mol. Sci. 2025, 26(21), 10293; https://doi.org/10.3390/ijms262110293 - 22 Oct 2025
Viewed by 403
Abstract
Carotid artery intima–media thickness (cIMT), a pre-clinical vascular change that accompanies atherosclerosis is considered as a cardiovascular risk factor. Coagulation factor XIII (FXIII) stabilizes the fibrin clot and increases its resistance to fibrinolysis. Regarding FXIII Val34Leu polymorphism, the protective effect of the Leu34 [...] Read more.
Carotid artery intima–media thickness (cIMT), a pre-clinical vascular change that accompanies atherosclerosis is considered as a cardiovascular risk factor. Coagulation factor XIII (FXIII) stabilizes the fibrin clot and increases its resistance to fibrinolysis. Regarding FXIII Val34Leu polymorphism, the protective effect of the Leu34 allele in the presence of elevated fibrinogen levels against myocardial infarction was demonstrated. Our aim was to investigate the effect of FXIII polymorphisms on cIMT. Patients with obesity (n = 69), type 2 diabetes mellitus (T2DM) (n = 104), and age- and sex-matched healthy controls (n = 82) were enrolled. FXIII polymorphisms (Val34Leu, His95Arg, Intron-K C>G) were determined by RT-PCR with FRET detection and melting curve analysis. cIMT was determined by B-mode ultrasound. Differences in cIMT between control (median: 0.5965, IQR: 0.5115–0.6580 mm) and T2DM (median: 0.7105, IQR: 0.5948–0.7568 mm), as well as between obese (median: 0.6105, IQR: 0.5455–0.6780 mm) and diabetic groups, were found (p < 0.0001 and p = 0.003, respectively). Genotype and allele frequencies of the studied polymorphisms did not differ between subgroups. In the study group (n = 255) after adjustment for age and sex, the presence of Intron-K G allele showed a significant and independent protective effect against cIMT progression in a separate model (p = 0.005) and after adjusting for other parameters associated with cIMT (p = 0.015). FXIII Intron-K G allele provides a protective effect against subclinical vascular disease in the studied population, and this effect is independent of the presence of obesity, as well as T2DM, Leu34 allele, and fibrinogen levels. Full article
(This article belongs to the Special Issue New Cardiovascular Risk Factors: 2nd Edition)
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Review

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15 pages, 798 KB  
Review
Angiotensin II and Atherosclerosis: A New Cardiovascular Risk Factor Beyond Hypertension
by Nicola Morat, Giovanni Civieri, Matteo Spezia, Mirko Menegolo, Giacomo Bernava, Sabino Iliceto, Laura Iop and Francesco Tona
Int. J. Mol. Sci. 2025, 26(15), 7527; https://doi.org/10.3390/ijms26157527 - 4 Aug 2025
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Abstract
The pivotal role of angiotensin II (AngII) in cardiovascular disease has been firmly established, as evidenced by a robust body of literature and the broad clinical application of AngII-inhibiting therapies. AngII type 1 receptor is the primary mediator of AngII action, and its [...] Read more.
The pivotal role of angiotensin II (AngII) in cardiovascular disease has been firmly established, as evidenced by a robust body of literature and the broad clinical application of AngII-inhibiting therapies. AngII type 1 receptor is the primary mediator of AngII action, and its activation initiates a multitude of cellular responses that contribute to the development of hypertension, structural changes in the heart and vasculature, and damage to target organs. This review examines AngII from a different perspective, exploring the link between the renin–angiotensin–aldosterone system and cardiovascular risk beyond hypertension, with particular emphasis on atherosclerosis development and progression. Full article
(This article belongs to the Special Issue New Cardiovascular Risk Factors: 2nd Edition)
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13 pages, 687 KB  
Review
Low LDL-Cholesterol and Hemorrhagic Risk: Mechanistic Insights and Clinical Perspectives
by Carmine Siniscalchi, Manuela Basaglia, Tiziana Meschi, Egidio Imbalzano, Francesca Futura Bernardi, Alessandro Perrella, Ugo Trama, Angelica Passannanti, Pierpaolo Di Micco and Concetta Schiano
Int. J. Mol. Sci. 2025, 26(12), 5612; https://doi.org/10.3390/ijms26125612 - 11 Jun 2025
Cited by 3 | Viewed by 3132
Abstract
Low-density lipoprotein cholesterol (LDL-C) plays a central role in lipid metabolism and is a well-established therapeutic target for the prevention of atherosclerotic cardiovascular diseases (CVDs). In recent years, increasingly aggressive lipid-lowering strategies have been adopted to achieve ultra-low LDL-C concentrations (<55 mg/dL or [...] Read more.
Low-density lipoprotein cholesterol (LDL-C) plays a central role in lipid metabolism and is a well-established therapeutic target for the prevention of atherosclerotic cardiovascular diseases (CVDs). In recent years, increasingly aggressive lipid-lowering strategies have been adopted to achieve ultra-low LDL-C concentrations (<55 mg/dL or even <30 mg/dL) in high-risk patients. While the benefits of LDL-C reduction in lowering the incidence of myocardial infarction and ischemic stroke are well documented, emerging clinical evidence has raised concerns about a potential association between very low LDL-C levels and an increased risk of bleeding, particularly hemorrhagic stroke and gastrointestinal hemorrhage. This review critically examines the molecular mechanisms by which reduced LDL-C levels may influence the hemostatic system and vascular integrity. It explores the complex interplay between cholesterol availability and platelet function, endothelial barrier stability, and coagulation pathways. In addition, we assess experimental and clinical studies supporting this association and discuss how these findings may inform risk stratification and personalized lipid-lowering strategies. A deeper understanding of the biological basis of this paradoxical risk is essential for achieving a safe, balanced, and effective approach to cardiovascular prevention. Full article
(This article belongs to the Special Issue New Cardiovascular Risk Factors: 2nd Edition)
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17 pages, 1935 KB  
Review
Non-Hypertensive Effects of Aldosterone
by Natalia Ekman, Ashley B. Grossman, Anna Nieckarz, Łukasz Jędrzejewski, Jacek Wolf and Dorota Dworakowska
Int. J. Mol. Sci. 2025, 26(2), 540; https://doi.org/10.3390/ijms26020540 - 10 Jan 2025
Cited by 5 | Viewed by 4355
Abstract
Aldosterone, the primary adrenal mineralocorticoid hormone, as an integral part of the renin–angiotensin–aldosterone system (RAAS), is crucial in blood pressure regulation and maintaining sodium and potassium levels. It interacts with the mineralocorticoid receptor (MR) expressed in the kidney and promotes sodium and water [...] Read more.
Aldosterone, the primary adrenal mineralocorticoid hormone, as an integral part of the renin–angiotensin–aldosterone system (RAAS), is crucial in blood pressure regulation and maintaining sodium and potassium levels. It interacts with the mineralocorticoid receptor (MR) expressed in the kidney and promotes sodium and water reabsorption, thereby increasing blood pressure. However, MRs are additionally expressed in other cells, such as cardiomyocytes, the endothelium, neurons, or brown adipose tissue cells. Therefore, aldosterone (especially aldosterone excess) may have other major impacts besides simply regulating blood pressure and circulating ion balance. Recent studies have reported a non-hypertensive impact on the cardiovascular, immune, and metabolic systems, a pro-oxidant effect, and a pro-fibrotic effect. In this review, we emphasise the non-hypertension-related effects of aldosterone, including advances in our understanding of the cellular mechanisms by which aldosterone mediates its cellular effects. We also summarise potential clinical complications related to both the hypertensive and non-hypertensive effects of aldosterone. Full article
(This article belongs to the Special Issue New Cardiovascular Risk Factors: 2nd Edition)
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