Submit to Biomedicines Review for Biomedicines Propose a Special Issue

Journal Browser

Molecular and Cellular Mechanisms of Cardiovascular Diseases

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 7509

Share This Special Issue

Special Issue Editors

Dr. Antonella Galeone

E-Mail Website
Guest Editor

Department of Surgery, Dentistry, Pediatrics and Gynecology, Division of Cardiac Surgery, University of Verona, 37134 Verona, Italy
Interests: aortic valve calcification; myocardial ischemia–reperfusion injury; heart failure; heart transplanta-tion
Special Issues, Collections and Topics in MDPI journals

Dr. Giacomina Brunetti

E-Mail Website
Guest Editor

Department of Biosciences, Biotechnologies, and Environment, University of Bari, Piazza Giulio Cesare, 11, 70124 Bari, Italy
Interests: osteoimmunology; osteoclast; osteoblast; bone remodeling; bone diseases; cardiovascular disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are a leading cause of death worldwide. The Special Issue “Molecular and Cellular Mechanisms of Cardiovascular Disease” will focus on the pathophysiology of cardiovascular disorders including, but not limited to, hypertension, diabetes, coronary artery disease, valvular heart disease, infective endocarditis, aortic dissection and aneurysms, heart failure, congenital and acquired cardiomyopathies, and cardiac tumors. This Special Issue will focus on the known and new signaling pathways involved in the large spectrum of cardiovascular diseases, affecting calcium homeostasis, mitochondria and energy metabolism, oxidative stress, inflammation, cardiac cell survival and apoptosis, autophagy and the extracellular matrix. In addition, the alteration of hormonal and neurohormonal signaling, including adrenergic systems, renin–angiotensin–aldosterone systems, and sex hormones, as well as the molecular and cellular mechanisms leading to gender differences in cardiovascular disease will be included in this Special Issue. This Special Issue aims to provide a better understanding of the molecular and cellular mechanisms that lead to cardiovascular disease that have not yet been fully elucidated. Furthermore, our aim is to gain a general overview of the known and new therapeutic approaches and drug targets in the field. Comprehensive reviews and original research (basic, translational, or clinical research), providing new insights into the molecular and cellular mechanisms leading to cardiovascular disease, including novel therapeutic approaches, are welcome.

Dr. Antonella Galeone
Dr. Giacomina Brunetti
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

hypertension
diabetes
coronary heart disease
valvular heart disease
infective endocarditis
aortic dissection
aortic aneurysm
heart failure
cardiomyopathy

Published Papers (6 papers)

Download All Papers

Research

Jump to: Review

15 pages, 2862 KiB

Open AccessArticle

Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis

by Ioan Alexandru Balmos, Mark Slevin, Klara Brinzaniuc, Adrian Vasile Muresan, Horatiu Suciu, Gyopár Beáta Molnár, Adriana Mocian, Béla Szabó, Előd Ernő Nagy and Emőke Horváth

Biomedicines 2023, 11(12), 3275; https://doi.org/10.3390/biomedicines11123275 - 11 Dec 2023

Viewed by 1006

Abstract

Background: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. Methods: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation. Results: Patients with intraplaque hemorrhage had greater CD68+ macrophage infiltration (p = 0.003). In 12 cases where iNOS2 predominated over Arg1 positivity, the occurrence of atherothrombotic events was significantly more frequent (p = 0.046). CD31 expression, representing neovessel formation, correlated positively with atherothrombosis (p = 0.020). Conclusions: Intraplaque hemorrhage is often described against the background of an intense inflammatory cell infiltrate. Atherothrombosis is associated with the presence of neovessels and pro-inflammatory macrophages expressing iNOS2. Modulating macrophage polarization may be a successful therapeutic approach to prevent plaque destabilization. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures

Graphical abstract

10 pages, 2172 KiB

Open AccessCommunication

HIF-2α Controls Expression and Intracellular Trafficking of the α2-Subunit of Na,K-ATPase in Hypoxic H9c2 Cardiomyocytes

by Emel Baloglu

Biomedicines 2023, 11(11), 2879; https://doi.org/10.3390/biomedicines11112879 - 24 Oct 2023

Viewed by 982

Abstract

The Na,K-ATPase (NKA) pump plays essential roles for optimal function of the heart. NKA activity decreases in necropsy materials from ischemic heart disease, heart failure and in experimental models. Cellular adaptation to hypoxia is regulated by hypoxia-induced transcription factors (HIF); we tested whether HIFs are involved in regulating the expression and intracellular dynamics of the α2-isoform of NKA (α2-NKA). HIF-1α and HIF-2α expression was suppressed in H9c2 cardiomyocytes by adenoviral infection, where cells were kept in 1% O₂ for 24 h. The silencing efficiency of HIFs was tested on the mRNA and protein expression. We measured the mRNA expression of α2-NKA in HIF-silenced and hypoxia-exposed cells. The membrane and intracellular expression of α2-NKA was measured after labelling the cell surface with NHS-SS-biotin, immunoprecipitation and Western blotting. Hypoxia increased the mRNA expression of α2-NKA 5-fold compared to normoxic cells in an HIF-2α-sensitive manner. The plasma membrane expression of α2-NKA increased in hypoxia by 2-fold and was fully prevented by HIF-2α silencing. Intracellular expression of α2-NKA was not affected. These results showed for the first time that in hypoxic cardiomyocytes α2-NKA is transcriptionally and translationally regulated by HIF-2α. The molecular mechanism behind this regulation needs further investigation. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures

Figure 1

Review

Jump to: Research

13 pages, 1831 KiB

Open AccessReview

Long Telomeric Repeat-Containing RNA (TERRA): Biological Functions and Challenges in Vascular Aging and Disease

by Paola Canale, Jonica Campolo, Andrea Borghini and Maria Grazia Andreassi

Biomedicines 2023, 11(12), 3211; https://doi.org/10.3390/biomedicines11123211 - 3 Dec 2023

Viewed by 1131

Abstract

Telomere dysfunction is implicated in vascular aging and shorter leucocyte telomeres are associated with an increased risk of atherosclerosis, myocardial infarction, and heart failure. Another pathophysiological mechanism that explains the causal relationship between telomere shortening and atherosclerosis development focuses on the clonal hematopoiesis of indeterminate potential (CHIP), which represents a new and independent risk factor in atherosclerotic cardiovascular diseases. Since telomere attrition has a central role in driving vascular senescence, understanding telomere biology is essential to modulate the deleterious consequences of vascular aging and its cardiovascular disease-related manifestations. Emerging evidence indicates that a class of long noncoding RNAs transcribed at telomeres, known as TERRA for “TElomeric Repeat-containing RNA”, actively participates in the mechanisms regulating telomere maintenance and chromosome end protection. However, the multiple biological functions of TERRA remain to be largely elucidated. In particular, the role of TERRA in vascular biology is surprisingly unknown. In this review, we discuss the current knowledge of TERRA and its roles in telomere biology. Additionally, we outline the pieces of evidence that exist regarding the relationship between TERRA dysregulation and disease. Finally, we speculate on how a comprehensive understanding of TERRA transcription in the cardiovascular system may provide valuable insights into telomere-associated vascular aging, offering great potential for new therapeutic approaches. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures

Graphical abstract

20 pages, 1443 KiB

Open AccessReview

Molecular Processes Involved in the Shared Pathways between Cardiovascular Diseases and Diabetes

by Julita Tokarek, Emilian Budny, Maciej Saar, Kamila Stańczak, Ewa Wojtanowska, Ewelina Młynarska, Jacek Rysz and Beata Franczyk

Biomedicines 2023, 11(10), 2611; https://doi.org/10.3390/biomedicines11102611 - 23 Sep 2023

Cited by 1 | Viewed by 898

Abstract

Cardiovascular diseases and diabetes mellitus are currently among the diseases with the highest morbidity and mortality. The pathogenesis and development of these diseases remain strongly connected, along with inflammation playing a major role. Therefore, the treatment possibilities showing a positive impact on both of these diseases could be especially beneficial for patients. SGLT-2 inhibitors and GLP-1 receptor agonists present this dual effect. Moreover, the hostile composition of the gut microbiota could influence the progression of these conditions. In this review, the authors present the latest knowledge on and innovations in diabetes mellitus and CVD—with the focus on the molecular mechanisms and the role of the microbiota. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures

Figure 1

18 pages, 1026 KiB

Open AccessReview

Brugada Syndrome: More than a Monogenic Channelopathy

by Antonella Liantonio, Matteo Bertini, Antonietta Mele, Cristina Balla, Giorgia Dinoi, Rita Selvatici, Marco Mele, Annamaria De Luca, Francesca Gualandi and Paola Imbrici

Biomedicines 2023, 11(8), 2297; https://doi.org/10.3390/biomedicines11082297 - 18 Aug 2023

Cited by 2 | Viewed by 1271

Abstract

Brugada syndrome (BrS) is an inherited cardiac channelopathy first diagnosed in 1992 but still considered a challenging disease in terms of diagnosis, arrhythmia risk prediction, pathophysiology and management. Despite about 20% of individuals carrying pathogenic variants in the SCN5A gene, the identification of a polygenic origin for BrS and the potential role of common genetic variants provide the basis for applying polygenic risk scores for individual risk prediction. The pathophysiological mechanisms are still unclear, and the initial thinking of this syndrome as a primary electrical disease is evolving towards a partly structural disease. This review focuses on the main scientific advancements in the identification of biomarkers for diagnosis, risk stratification, pathophysiology and therapy of BrS. A comprehensive model that integrates clinical and genetic factors, comorbidities, age and gender, and perhaps environmental influences may provide the opportunity to enhance patients’ quality of life and improve the therapeutic approach. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures

Figure 1

17 pages, 1030 KiB

Open AccessReview

The ST2/IL-33 Pathway in Adult and Paediatric Heart Disease and Transplantation

by Giacomina Brunetti, Barbara Barile, Grazia Paola Nicchia, Francesco Onorati, Giovanni Battista Luciani and Antonella Galeone

Biomedicines 2023, 11(6), 1676; https://doi.org/10.3390/biomedicines11061676 - 9 Jun 2023

Cited by 5 | Viewed by 1524

Abstract

ST2 is a member of interleukin 1 receptor family with soluble sST2 and transmembrane ST2L isoforms. The ligand of ST2 is IL-33, which determines the activation of numerous intracytoplasmic mediators following the binding with ST2L and IL-1RAcP, leading to nuclear signal and cardiovascular effect. Differently, sST2 is released in the blood and works as a decoy receptor, binding IL-33 and blocking IL-33/ST2L interaction. sST2 is mainly involved in maintaining homeostasis and/or alterations of different tissues, as counterbalance/activation of IL-33/ST2L axis is typically involved in the development of fibrosis, tissue damage, inflammation and remodeling. sST2 has been described in different clinical reports as a fundamental prognostic marker in patients with cardiovascular disease, as well as marker for the treatment monitoring of patients with heart failure; however, further studies are needed to better elucidate its role. In this review we reported the current knowledge about its role in coronary artery disease, heart failure, heart transplantation, heart valve disease, pulmonary arterial hypertension, and cardiovascular interventions. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases)

► Show Figures