Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

New Cardiovascular Risk Factors

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Related Special Issue
Published Papers

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: closed (20 September 2024) | Viewed by 15053

Share This Special Issue

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 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 the reduction in cardiovascular risk.

Dr. Antonio Barbato
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

atherosclerosis
cardiovascular risk
arterial stiffness
blood pressure
vitamin D
miRNA
inflammation

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

New Cardiovascular Risk Factors: 2nd Edition in International Journal of Molecular Sciences

Published Papers (8 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

12 pages, 538 KiB

Open AccessArticle

Genetic Associations of Plasminogen Activator Inhibitor-1-Related miRNA Variants with Coronary Artery Disease

by Yong Hyun Ha, Jung Hoon Sung, Chang Soo Ryu, Eun Ju Ko, Hyeon Woo Park, Han Sung Park, Ok Joon Kim, In Jai Kim and Nam Keun Kim

Int. J. Mol. Sci. 2024, 25(21), 11528; https://doi.org/10.3390/ijms252111528 - 27 Oct 2024

Viewed by 603

Abstract

Coronary artery disease (CAD) is one of the most common types of cardiovascular disease and can lead to a heart attack as plaque gradually builds up inside the coronary arteries, blocking blood flow. Previous studies have shown that polymorphisms in the PAI-1 gene are associated with CAD; however, studies of the PAI-1 3′-untranslated region, containing a miRNA binding site, and the miRNAs that interact with it, are insufficient. To investigate the association between miRNA polymorphisms and CAD in the Korean population based on post-transcriptional regulation, we genotyped five polymorphisms in four miRNAs targeting the 3′-untranslated region of PAI-1 using real-time PCR and TaqMan assays. We found that the mutant genotype of miR-30c rs928508 A > G was strongly associated with increased CAD susceptibility. In a genotype combination analysis, the combination of the homozygous mutant genotype (GG) of miR-30c rs928508 with the wild-type genotype (GG) of miR-143 rs41291957 resulted in increased risk for CAD. Also, in an allele combination analysis, the combination of the mutant allele (G) of miR-30c rs928508 and the wild-type allele (G) of miR-143 rs41291957 resulted in increased risk for CAD. Furthermore, metabolic syndrome and diabetes mellitus showed synergistic effects on CAD risk when combined with miR-30c rs928508. These results can be applied to identify CAD prognostic biomarkers among miRNA polymorphisms and various clinical factors. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

17 pages, 1038 KiB

Open AccessArticle

Intestinal Microbiota and Derived Metabolites in Myocardial Fibrosis and Postoperative Atrial Fibrillation

by Antonio Nenna, Alice Laudisio, Chiara Taffon, Marta Fogolari, Cristiano Spadaccio, Chiara Ferrisi, Francesco Loreni, Omar Giacinto, Ciro Mastroianni, Raffaele Barbato, David Rose, Antonio Salsano, Francesco Santini, Silvia Angeletti, Anna Crescenzi, Raffaele Antonelli Incalzi, Massimo Chello and Mario Lusini

Int. J. Mol. Sci. 2024, 25(11), 6037; https://doi.org/10.3390/ijms25116037 - 30 May 2024

Viewed by 940

Abstract

The high incidence of atrial fibrillation (AFib) following cardiac surgery (postoperative atrial fibrillation, POAF) relies on specific surgical features. However, in the setting of POAF, the role of the microbiome in the modulation of cardiac fibrosis is still not clear. This study aimed to analyze the effect of the microbiome and its main metabolic product (trimethylamine-N-oxide, TMAO) in the fibrosis of myocardial tissue, to investigate its role in POAF. Patients undergoing elective cardiac surgery with cardiopulmonary bypass, central atrio-caval cannulation and no history of AFib, were included. A fragment of the right atrium was analyzed for qualitative and mRNA-quantitative evaluation. A preoperative blood sample was analyzed with enzyme-linked immunosorbent assay (ELISA). A total of 100 patients have been included, with POAF occurring in 38%. Histologically, a higher degree of fibrosis, angiogenesis and inflammation has been observed in POAF. Quantitative evaluation showed increased mRNA expression of collagen-1, collagen-3, fibronectin, and transforming growth factor beta (TGFb) in the POAF group. ELISA analysis showed higher levels of TMAO, lipopolysaccharide and TGFb in POAF, with similar levels of sP-selectin and zonulin. TMAO ≥ 61.8 ng/mL (odds ratio, OR 2.88 [1.35–6.16], p = 0.006), preoperative hemoglobin < 13.1 g/dL (OR 2.37 [1.07–5.24], p = 0.033) and impaired right ventricular function (OR 2.38 [1.17–4.83], p = 0.017) were independent predictors of POAF. Also, TMAO was significantly associated with POAF by means of increased fibrosis. Gut microbiome product TMAO is crucial for myocardial fibrosis, which is a key factor for POAF. Patients in preoperative sinus rhythm who will develop POAF have increased genetic expression of pro-fibrotic genes and enhanced fibrosis in histological staining. Elevated TMAO level (≥61.8 ng/mL) is an independent risk factor for POAF. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

11 pages, 2380 KiB

Open AccessArticle

Isolated Valve Amyloid Deposition in Aortic Stenosis: Potential Clinical and Pathophysiological Relevance

by Maddalena Conte, Paolo Poggio, Maria Monti, Laura Petraglia, Serena Cabaro, Dario Bruzzese, Giuseppe Comentale, Aurelio Caruso, Mariagabriella Grimaldi, Emilia Zampella, Annarita Gencarelli, Maria Rosaria Cervasio, Flora Cozzolino, Vittoria Monaco, Veronika Myasoedova, Vincenza Valerio, Adele Ferro, Luigi Insabato, Michele Bellino, Gennaro Galasso, Francesca Graziani, Pietro Pucci, Pietro Formisano, Emanuele Pilato, Alberto Cuocolo, Pasquale Perrone Filardi, Dario Leosco and Valentina Parisi Show full author list Hide full author list

Int. J. Mol. Sci. 2024, 25(2), 1171; https://doi.org/10.3390/ijms25021171 - 18 Jan 2024

Cited by 3 | Viewed by 1364

Abstract

Amyloid deposition within stenotic aortic valves (AVs) also appears frequent in the absence of cardiac amyloidosis, but its clinical and pathophysiological relevance has not been investigated. We will elucidate the rate of isolated AV amyloid deposition and its potential clinical and pathophysiological significance in aortic stenosis (AS). In 130 patients without systemic and/or cardiac amyloidosis, we collected the explanted AVs during cardiac surgery: 57 patients with calcific AS and 73 patients with AV insufficiency (41 with AV sclerosis and 32 without, who were used as controls). Amyloid deposition was found in 21 AS valves (37%), 4 sclerotic AVs (10%), and none of the controls. Patients with and without isolated AV amyloid deposition had similar clinical and echocardiographic characteristics and survival rates. Isolated AV amyloid deposition was associated with higher degrees of AV fibrosis (p = 0.0082) and calcification (p < 0.0001). Immunohistochemistry analysis suggested serum amyloid A1 (SAA1), in addition to transthyretin (TTR), as the protein possibly involved in AV amyloid deposition. Circulating SAA1 levels were within the normal range in all groups, and no difference was observed in AS patients with and without AV amyloid deposition. In vitro, AV interstitial cells (VICs) were stimulated with interleukin (IL)-1β which induced increased SAA1-mRNA both in the control VICs (+6.4 ± 0.5, p = 0.02) and the AS VICs (+7.6 ± 0.5, p = 0.008). In conclusion, isolated AV amyloid deposition is frequent in the context of AS, but it does not appear to have potential clinical relevance. Conversely, amyloid deposition within AV leaflets, probably promoted by local inflammation, could play a role in AS pathophysiology. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

16 pages, 1904 KiB

Open AccessArticle

Relation of Plasma Catecholamine Concentrations and Myocardial Mitochondrial Respiratory Activity in Anesthetized and Mechanically Ventilated, Cardiovascular Healthy Swine

by Nadja Abele, Franziska Münz, Fabian Zink, Michael Gröger, Andrea Hoffmann, Eva-Maria Wolfschmitt, Melanie Hogg, Enrico Calzia, Christiane Waller, Peter Radermacher and Tamara Merz

Int. J. Mol. Sci. 2023, 24(24), 17293; https://doi.org/10.3390/ijms242417293 - 9 Dec 2023

Cited by 1 | Viewed by 1217

Abstract

Chronic heart failure is associated with reduced myocardial β-adrenergic receptor expression and mitochondrial function. Since these data coincide with increased plasma catecholamine levels, we investigated the relation between myocardial β-receptor expression and mitochondrial respiratory activity under conditions of physiological catecholamine concentrations. This post hoc analysis used material of a prospective randomized, controlled study on 12 sexually mature (age 20–24 weeks) Early Life Stress or control pigs (weaning at day 21 and 28–35 after birth, respectively) of either sex. Measurements in anesthetized, mechanically ventilated, and instrumented animals comprised serum catecholamine (liquid-chromatography/tandem-mass-spectrometry) and 8-isoprostane levels, whole blood superoxide anion concentrations (electron spin resonance), oxidative DNA strand breaks (tail moment in the “comet assay”), post mortem cardiac tissue mitochondrial respiration, and immunohistochemistry (β₂-adrenoreceptor, mitochondrial respiration complex, and nitrotyrosine expression). Catecholamine concentrations were inversely related to myocardial mitochondrial respiratory activity and β₂-adrenoceptor expression, whereas there was no relation to mitochondrial respiratory complex expression. Except for a significant, direct, non-linear relation between DNA damage and noradrenaline levels, catecholamine concentrations were unrelated to markers of oxidative stress. The present study suggests that physiological variations of the plasma catecholamine concentrations, e.g., due to physical and/or psychological stress, may affect cardiac β₂-adrenoceptor expression and mitochondrial respiration. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

15 pages, 1771 KiB

Open AccessArticle

Cardioprotective and Antifibrotic Effects of Low-Dose Renin–Angiotensin–Aldosterone System Inhibitors in Type 1 Diabetic Rat Model

by Dora B. Balogh, Agnes Molnar, Arianna Degi, Akos Toth, Lilla Lenart, Adar Saeed, Adrienn Barczi, Attila J. Szabo, Laszlo J. Wagner, Gyorgy Reusz and Andrea Fekete

Int. J. Mol. Sci. 2023, 24(23), 17043; https://doi.org/10.3390/ijms242317043 - 1 Dec 2023

Cited by 4 | Viewed by 1705

Abstract

Diabetic cardiovascular complications are associated with up to 50% mortality, and current therapies are not effective enough. Renin–angiotensin–aldosterone system inhibitors (RAASis) are the standard of care for diabetic patients with hypertension and albuminuria. Based on our previous studies reporting the renoprotective effects of low-dose RAASis, here, we hypothesized that low-dose RAASi treatment has cardioprotective and antifibrotic benefits in type 1 diabetes mellitus (T1DM). After five weeks of T1DM, adult male Wistar rats received low doses of ramipril, losartan, or eplerenone for two weeks. Heart rate, blood pressure, and pulse wave velocity (PWV) were recorded. Aortic intima–media thickness (IMT), collagen accumulation, and myocardial fibrosis were assessed. All RAASis reduced PWV elevation, prevented the progression of myocardial fibrosis, and normalized B-type natriuretic peptide, troponin I, and fibroblast growth factor 23 levels without affecting blood pressure. Interestingly, only eplerenone reversed the decline in Klotho levels and reduced IMT and fibrosis in the media of the aorta. Our comparative analysis suggests that mineralocorticoid receptor antagonists, particularly eplerenone, may offer superior efficacy in halting both the arterial and the myocardial injuries in T1DM compared to angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor blockers. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

Review

Jump to: Research

29 pages, 2224 KiB

Open AccessReview

Inflammation, Oxidative Stress, and Endothelial Dysfunction in the Pathogenesis of Vascular Damage: Unraveling Novel Cardiovascular Risk Factors in Fabry Disease

by Denise Cristiana Faro, Francesco Lorenzo Di Pino and Ines Paola Monte

Int. J. Mol. Sci. 2024, 25(15), 8273; https://doi.org/10.3390/ijms25158273 - 29 Jul 2024

Cited by 1 | Viewed by 1751

Abstract

Anderson-Fabry disease (AFD), a genetic disorder caused by mutations in the α-galactosidase-A (GLA) gene, disrupts lysosomal function, leading to vascular complications. The accumulation of globotriaosylceramide (Gb3) in arterial walls triggers upregulation of adhesion molecules, decreases endothelial nitric oxide synthesis, and induces reactive oxygen species production. This cascade results in fibrotic thickening, endothelial dysfunction, hypercontractility, vasospasm, and a pro-thrombotic phenotype. AFD patients display increased intima-media thickness (IMT) and reduced flow-mediated dilation (FMD), indicating heightened cardiovascular risk. Nailfold capillaroscopy (NFC) shows promise in diagnosing and monitoring microcirculatory disorders in AFD, though it remains underexplored. Morphological evidence of AFD as a storage disorder can be demonstrated through electron microscopy and immunodetection of Gb3. Secondary pathophysiological disturbances at cellular, tissue, and organ levels contribute to the clinical manifestations, with prominent lysosomal inclusions observed in vascular, cardiac, renal, and neuronal cells. Chronic accumulation of Gb3 represents a state of ongoing toxicity, leading to increased cell turnover, particularly in vascular endothelial cells. AFD-related vascular pathology includes increased renin-angiotensin system activation, endothelial dysfunction, and smooth muscle cell proliferation, resulting in IMT increase. Furthermore, microvascular alterations, such as atypical capillaries observed through NFC, suggest early microvascular involvement. This review aims to unravel the complex interplay between inflammation, oxidative stress, and endothelial dysfunction in AFD, highlighting the potential connections between metabolic disturbances, oxidative stress, inflammation, and fibrosis in vascular and cardiac complications. By exploring novel cardiovascular risk factors and potential diagnostic tools, we can advance our understanding of these mechanisms, which extend beyond sphingolipid accumulation to include other significant contributors to disease pathogenesis. This comprehensive approach can pave the way for innovative therapeutic strategies and improved patient outcomes. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

17 pages, 1266 KiB

Open AccessReview

New Modifiable Risk Factors Influencing Coronary Artery Disease Severity

by Kamila Florek, Maja Kübler, Magdalena Górka and Piotr Kübler

Int. J. Mol. Sci. 2024, 25(14), 7766; https://doi.org/10.3390/ijms25147766 - 16 Jul 2024

Cited by 1 | Viewed by 1404

Abstract

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide with coronary artery disease (CAD) being the first culprit in this group. In terms of CAD, not only its presence but also its severity plays a role in the patient’s treatment and prognosis. CAD complexity can be assessed with the indicator named the SYNTAX score (SS). A higher SS is associated with major adverse cardiovascular event (MACE) occurrence in short- and long-term observations. Hence, the risk factors affecting CAD severity based on SS results may help lower the risk among patients with already developed CAD to reduce their impact on coronary atherosclerosis progression. The well-established risk factors of CAD are consistent with those associated with the coronary plaque burden. However, recently, it was shown that new indicators exist, which we present in this paper, that significantly contribute to CAD complexity such as inflammatory parameters, C-reactive protein (CRP), ratios based on blood smear results, and uric acid. Moreover, microbiota alteration, vitamin D deficiency, and obstructive sleep apnea (OSA) also predicted CAD severity. However, sometimes, certain indicators were revealed as significant only in terms of chronic coronary syndromes (CCSs) or specific acute coronary syndromes (ACSs). Importantly, there is a need to apply the interdisciplinary and translational approach to the novel CAD severity risk assessment to maximize the impact of secondary prevention among patients at risk of coronary atherosclerosis progression. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Figure 1

24 pages, 1723 KiB

Open AccessReview

New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review

by Jorge E. Jalil, Luigi Gabrielli, María Paz Ocaranza, Paul MacNab, Rodrigo Fernández, Bruno Grassi, Paulina Jofré, Hugo Verdejo, Monica Acevedo, Samuel Cordova, Luis Sanhueza and Douglas Greig

Int. J. Mol. Sci. 2024, 25(8), 4407; https://doi.org/10.3390/ijms25084407 - 17 Apr 2024

Cited by 4 | Viewed by 5175

Abstract

This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans. Full article

(This article belongs to the Special Issue New Cardiovascular Risk Factors)

► Show Figures

Journal Menu

Journal Browser

New Cardiovascular Risk Factors

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Related Special Issue

Published Papers (8 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI