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Molecular Diagnosis in Cardiovascular Diseases
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Molecular Diagnosis in Cardiovascular Diseases

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: closed (20 February 2026) | Viewed by 7584

Special Issue Editors

Prof. Dr. Calogera Pisano

E-Mail Website
Guest Editor
Cardiac Surgery Unit, Department of Precision Medicine in Medical Surgical and Critical Area (Me.Pre.C.C.), University of Palermo, 90134 Palermo, Italy
Interests: aneurysm; cardiac surgery; heart failure
Dr. Carmela Rita Balistreri

E-Mail Website
Guest Editor
Cellular, Molecular and Clinical Pathological Laboratory, Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), University of Palermo, 90134 Palermo, Italy
Interests: genetic and pathology of aortopathy and cerebrovascular diseases; inflammatpry diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppe Raffa

E-Mail Website
Guest Editor
Department of Cardiac Surgery, Istituto Mediterraneo per i Trapianti e Terapia ad Alta Specializzazione-IRCCS-ISMETT, UPMC Italy, Palermo, Italy
Interests: aneurysm; heart failure

Special Issue Information

Dear Colleagues,

Cardiac diseases form the majority of the global disease burden, owing to the paradigm shift from infectious diseases to non-infectious diseases. The prevalence of CVDs has nearly doubled, increasing from 271 million in 1990 to 523 million in 2019. The advent of precision medicine in cardiology has ignited new possibilities for individually personalized, integrative, and patient-centric approaches to disease prevention and treatment. The major objective of this Special Issue was to compile the evolving relevant tools of precision medicine that can help with the evidence-based precise individualized diagnosis of cardiac diseases with the highest DALY. In particular, in this Special Issue, we analyse the role of precision medicine in the diagnosis of aortopathy and heart failure. We are also interested in inflammatory (TLR-4, interleukine, chemochine, linfocite) and non-inflammatory biomarkers (genetic patterns), in addition to the following  prognostic and diagnostic biomarkers of heart failure: NPs (natriuretic peptide), MR-proANP (mid-regional pro-atrial natriuretic peptide), IGFBP7 (insulin-like growth factor-binding protein 7), Procalcitonina, NPs (natriuretic peptide), hs-cTn (high-sensivity cardiac troponin), sST2 (soluble suppressor of tumorigenicity-2), Gal-3* (Galectina-3), NPs (natriuretic peptide), bio-ADM (bio-adrenomedullin), CA-125 (Cancer antigen 125) and DPP3 (Dipeptidyl peptidase 3).

Prof. Dr. Calogera Pisano
Dr. Carmela Rita Balistreri
Dr. Giuseppe Raffa
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 250 words) can be sent to the Editorial Office for assessment.

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

  • cardiac diseases
  • molecular diagnosis
  • aortopathy
  • aneurysm
  • dissection
  • heart failure

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Published Papers (4 papers)

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Research

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12 pages, 1305 KB  
Communication
The Role of Chemokines and Small Leucine-Rich Proteoglycans in Cardiac Remodeling in Immunosuppressant-Treated Male Rats
by Anna Surówka, Michał Żołnierczuk, Piotr Prowans, Marta Grabowska, Patrycja Kupnicka, Marta Markowska, Zbigniew Szlosser, Edyta Zagrodnik and Karolina Kędzierska-Kapuza
Int. J. Mol. Sci. 2025, 26(13), 6414; https://doi.org/10.3390/ijms26136414 - 3 Jul 2025
Viewed by 889
Abstract
Chemokines are low-molecular-weight peptides classified as cytokines with chemotactic properties. The chemokine CXCL13 and its receptor CXCR5 play a significant role in cardiac remodeling, and their expression is markedly increased in experimental models of heart failure. Increased CXCL13 activity is associated with the [...] Read more.
Chemokines are low-molecular-weight peptides classified as cytokines with chemotactic properties. The chemokine CXCL13 and its receptor CXCR5 play a significant role in cardiac remodeling, and their expression is markedly increased in experimental models of heart failure. Increased CXCL13 activity is associated with the expression of fibromodulin, a proteoglycan that binds and cross-links collagen fibers. The stressed heart undergoes intensive remodeling, including fibrosis. In our experiment, we investigated the effect of the most commonly used triple immunosuppressive regimens on the expression of the CXCR5 receptor, the chemokine CXCL13, and fibromodulin in rat heart tissue. For this purpose, we used Western blot analysis and ELISA. The study was started on 36 rats divided into 6 groups, which received drugs for a period of 6 months. Our results suggest that the chronic use of calcineurin inhibitors in combination with mycophenolate mofetil is a significant stress factor for the heart, leading to abnormal remodeling of the extracellular matrix. The use of rapamycin may alleviate the negative effects of immunosuppressive therapy on the heart. Our results are consistent with the results of our previous studies and provide a basis for further work aimed at understanding the pathophysiology of the development of changes in the heart with individual immunosuppressive regimens. Full article
(This article belongs to the Special Issue Molecular Diagnosis in Cardiovascular Diseases)
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Review

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18 pages, 573 KB  
Review
MicroRNA Signatures in Cardiometabolic Disorders as a Next-Generation Diagnostic Approach: Current Insight
by Concetta Iside, Francesca Picone, Paola Di Pietro, Angela Carmelita Abate, Valeria Prete, Antonio Damato, Eleonora Venturini, Saad Akeel, Salvatore Petralia, Carmine Vecchione and Albino Carrizzo
Int. J. Mol. Sci. 2025, 26(21), 10769; https://doi.org/10.3390/ijms262110769 - 5 Nov 2025
Cited by 2 | Viewed by 1188
Abstract
Cardiometabolic diseases, including cardiovascular disorders and type 2 diabetes mellitus, are the leading cause of morbidity and mortality worldwide, placing a significant burden on healthcare systems. Although advances in imaging and risk stratification have improved disease management, conventional diagnostic and prognostic tools often [...] Read more.
Cardiometabolic diseases, including cardiovascular disorders and type 2 diabetes mellitus, are the leading cause of morbidity and mortality worldwide, placing a significant burden on healthcare systems. Although advances in imaging and risk stratification have improved disease management, conventional diagnostic and prognostic tools often lack the requisite sensitivity and specificity for early and precise risk stratification. This limitation stems from their poor ability to capture the full molecular complexity of these conditions, underscoring an urgent need for innovative biomarkers to bridge these gaps. MicroRNAs, small non-coding RNAs that regulate gene expression post-transcriptionally, have emerged as promising candidates. Their characteristics offer several advantages over traditional methods, including exceptional stability in biological fluids, strong tissue and disease specificity, and the ability to reflect dynamic pathological changes. These unique features enable miRNAs to detect subtle molecular alterations that may precede clinical symptoms, thereby overcoming key limitations of current diagnostic approaches. Altered circulating miRNA profiles have been linked to pathological processes such as endothelial dysfunction, inflammation, oxidative stress, and maladaptive cardiac remodeling. This review provides a comprehensive overview of the current evidence supporting the diagnostic and prognostic role of circulating miRNAs in cardiometabolic disease. We highlight their potential as early detection biomarkers, tools for patient stratification, and indicators of therapeutic response. Furthermore, we discuss key limitations to clinical translation, including methodological variability, challenges in sample handling, differences in normalization strategies, and platform-dependent quantification inconsistencies. Overcoming these obstacles and achieving robust large-scale clinical validation will be essential to fully harness the potential of miRNAs as next-generation molecular signatures in precision medicine. Full article
(This article belongs to the Special Issue Molecular Diagnosis in Cardiovascular Diseases)
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23 pages, 2160 KB  
Review
Why Are Internal Mammary (Thoracic) Arteries Less Prone to Developing Atherosclerosis Compared to Coronary Arteries? Do Gut Microbiota Play a Role? A Narrative Review
by Leon M. T. Dicks
Int. J. Mol. Sci. 2025, 26(18), 9052; https://doi.org/10.3390/ijms26189052 - 17 Sep 2025
Cited by 1 | Viewed by 2712
Abstract
Atherosclerosis (AS), the leading cause of cardiovascular disease (CVD), is the thickening and stiffening of arterial walls, mainly of coronary arteries, the aorta, and the internal carotid artery. Blood flow is restricted by the deposit of lipid-rich macrophages (foam cells), calcium, fibrin, and [...] Read more.
Atherosclerosis (AS), the leading cause of cardiovascular disease (CVD), is the thickening and stiffening of arterial walls, mainly of coronary arteries, the aorta, and the internal carotid artery. Blood flow is restricted by the deposit of lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques on the inner lining (tunica intima) of arterial walls. Damaged endothelia become inflamed and accumulate macrophages, monocytes, granulocytes, and dendritic cells, which intensifies plaque formation and increases the risk of myocardial infarction (MI) and thrombosis. Many of the anatomical and physiological abnormalities in arterial walls can be linked to colonic bacteria that produce inflammation-inducing metabolites, e.g., succinate, fumarate, fatty acids (FAs), reactive oxygen species (ROS), lipopolysaccharides (LPS), and trimethylamine-N-oxide (TMAO). TMAO triggers platelet formation, inhibits the synthesis of bile acids (BAs), accelerates the formation of aortic lesions, and upregulates the expression of membrane glycoprotein CD36 (also known as platelet glycoprotein 4) on the surface of platelets and epithelial cells. The ability of internal mammary arteries (IMAs) to produce higher levels of apolipoprotein C-III (apo-CIII) and paraoxonase (PON), compared to coronary arteries, prevents plaque buildup. The tunica intima of IMAs is rich in heparin sulfate and endothelial nitric oxide synthase (eNOS). Increased production of NO relaxes VSMCs and suppresses GTP cyclohydrolase (GTPCH), which lowers blood pressure. Higher levels of prostacyclin (PG12) produced by IMAs inhibit platelet aggregation. IMAs are structurally different from coronary arteries by having a thinner, non-fenestrated, tunica intima without a prominent internal elastic lamina. These characteristics render IMAs ideal conduits in coronary artery bypass graft (CABG) surgery. This review provides information that may explain why IMAs are less affected by inflammatory reactions and more resilient to plaque formation. Full article
(This article belongs to the Special Issue Molecular Diagnosis in Cardiovascular Diseases)
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13 pages, 2526 KB  
Review
A Narrative Review: Syndecans in Aortic Aneurysm Pathogenesis and Course—Biomarkers and Targets?
by Calogera Pisano, Laura Asta, Adriana Sbrigata and Carmela Rita Balistreri
Int. J. Mol. Sci. 2025, 26(3), 1211; https://doi.org/10.3390/ijms26031211 - 30 Jan 2025
Cited by 5 | Viewed by 2267
Abstract
The maintenance of the integrity of the entire endothelium, glycocalyx included, and, therefore, of tissue aorta’s homeostasis, depends on the expressions of several molecular pathways and their interactions, such as syndecan molecules. Alterations in syndecans, i.e., quantitative alterations or linking to their shedding, [...] Read more.
The maintenance of the integrity of the entire endothelium, glycocalyx included, and, therefore, of tissue aorta’s homeostasis, depends on the expressions of several molecular pathways and their interactions, such as syndecan molecules. Alterations in syndecans, i.e., quantitative alterations or linking to their shedding, contributes to invoking endothelium dysfunction, which causes damage to the vessel wall due to the increased production of growth-stimulating and pro-inflammatory gene products. Inflammatory processes negatively affect the integrity of the endothelial glycocalyx, a dynamic layer of the luminal portion of endothelial cells composed of proteoglycans, glycoproteins, and glycosaminoglycans, i.e., syndecans. In turn, structural alterations in the endothelial glycocalyx influence the coagulative state, increasing pro-thrombotic processes. The family of syndecans constitutes a major component of glycocalyx or, more accurately, the major source of cell surface heparan sulfate. It encompasses four components: syndecan-1, syndecan-2, and syndecan-4 (with syndecan-3 only expressed in neural tissue), which have a fundamental role in regulating the events of acute and chronic aorta damage subsequently correlated with the formation of aneurysms. As such, the aim of our review is to highlight the current knowledge on the roles of syndecans and to analyze their relationship with the pathological processes of the aortic wall based on the most recent literature. Full article
(This article belongs to the Special Issue Molecular Diagnosis in Cardiovascular Diseases)
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