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Molecular Mechanisms and Treatment of Cardiovascular Diseases
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Molecular Mechanisms and Treatment of 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: 20 April 2025 | Viewed by 6929

Special Issue Editor

Dr. Lucia La Sala

E-Mail Website
Guest Editor
Department of Cardiovascular and Metabolic Diseases, IRCCS Multimedica, Via Fantoli 16/15, 20135 Milan, Italy
Interests: glycemic variability; redox systems; diabetes; insulin resistance; prediabetes; microRNA; extracellular vesicles; obesity; innate immune response; cutaneous and visceral adipose tissues; inflammation; signaling pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of this Special Issue is to collect high-quality research articles, review articles, short communications in the field of cardiovascular diseases, including but not limited to cell biology and molecular research. Meta-analysis of literature focused on the major aspects of cardiovascular diseases (CVDs) will be included in this Special Issue.

CVDs represent the main cause of morbidity and mortality in industrialized and developing countries, which are considered a real emergency worldwide. The prevention of cardiovascular diseases, through a series of combined actions aimed to interventions in risk factors and therapeutics able to reduce their burden, has unequivocally demonstrated a benefit in the reduction of adverse events with a reduction in healthcare costs. The known pathologies with a strong impact on cardiovascular and cerebrovascular functions, diabetes mellitus (DM) and some conditions frequently associated with it—such as obesity, high blood pressure, insulin resistance (IR)—represents the first cause of increased risk of cardiovascular events: more than half the mortality and a vast amount of morbidity in people with DM is related to CVD, including stroke disease and peripheral disease.

We encourage the submission of manuscripts that provide novel and mechanistic molecular insights and papers that report significant advances in the field.

Dr. Lucia La Sala
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

  • cardiovascular diseases
  • molecular pathology
  • microRNAs
  • diabetes
  • cardiovascular complications of diabetes

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Published Papers (4 papers)

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Research

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14 pages, 2058 KiB  
Article
Maternal Salivary miR-423-5p Is Linked to Neonatal Outcomes and Periodontal Status in Cardiovascular-High-Risk Pregnancies
by Lucia La Sala, Valentina Carlini, Chiara Mandò, Gaia Maria Anelli, Antonio E. Pontiroli, Emilio Trabucchi, Irene Cetin and Silvio Abati
Int. J. Mol. Sci. 2024, 25(16), 9087; https://doi.org/10.3390/ijms25169087 - 22 Aug 2024
Viewed by 836
Abstract
Periodontal disease (PD) during pregnancy may trigger systemic inflammation, increasing the risk of developing cardiometabolic disease (CMD). As a consequence, PD may result in the activation of cellular and molecular pathways, affecting the disease course and pregnancy outcome. Although microRNAs (miRNAs) are considered [...] Read more.
Periodontal disease (PD) during pregnancy may trigger systemic inflammation, increasing the risk of developing cardiometabolic disease (CMD). As a consequence, PD may result in the activation of cellular and molecular pathways, affecting the disease course and pregnancy outcome. Although microRNAs (miRNAs) are considered ideal biomarkers for many diseases, few studies have investigated salivary miRNAs and their role in pregnancy or neonatal outcomes. In this study, we sought to investigate the associations between salivary miRNAs of pregnant women with oral diseases and their effects on neonatal outcomes. Eleven (n = 11) salivary miRNAs from a cohort of pregnant women with oral diseases (n = 32; oral health, H; gingivitis, G; and periodontitis, P) were detected using a previous profiling analysis with an FDR < 0.20 and a fold change (FC) < 0.5 or FC > 2 for the most highly expressed miRNAs. Spearman correlations were performed for 11 salivary microRNAs associated with oral-derived inflammation, which could affect neonatal outcomes during pregnancies at risk for cardiometabolic disease (CMD), defined by the presence of a high pregestational BMI. In addition, ROC curves demonstrated the diagnostic accuracy of the markers used. Upregulation of miR-423-5p expression and a decrease in miR-27b-3p expression were detected in the P-group (p < 0.05), and ROC analysis revealed the diagnostic accuracy of miR-423-5p for discriminating oral diseases, such as gingivitis versus periodontitis (P vs. G, AUC = 0.78, p < 0.05), and for discriminating it from the healthy oral cavity (P vs. H, AUC = 0.9, p < 0.01). In addition, miR-27b-3p and miR-622 were also able to discriminate the healthy group from the P-group (AUC = 0.8, p < 0.05; AUC = 0.8, p < 0.05). miR-483-5p was able to discriminate between the G-group (AUC = 0.9, p < 0.01) and the P-group (AUC = 0.8, p < 0.05). These data support the role of salivary miRNAs as early biomarkers for neonatal outcomes in pregnant women with periodontal disease at high risk for CMD and suggest that there is cross-talk between salivary miRNAs and subclinical systemic inflammation. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Cardiovascular Diseases)
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16 pages, 2532 KiB  
Article
Protein Disulfide Isomerase 4 Is an Essential Regulator of Endothelial Function and Survival
by Shuhan Bu, Aman Singh, Hien C. Nguyen, Bharatsinai Peddi, Kriti Bhatt, Naresh Ravendranathan, Jefferson C. Frisbee and Krishna K. Singh
Int. J. Mol. Sci. 2024, 25(7), 3913; https://doi.org/10.3390/ijms25073913 - 31 Mar 2024
Cited by 2 | Viewed by 1227
Abstract
Endothelial autophagy plays an important role in the regulation of endothelial function. The inhibition of endothelial autophagy is associated with the reduced expression of protein disulfide isomerase 4 (PDIA-4); however, its role in endothelial cells is not known. Here, we report [...] Read more.
Endothelial autophagy plays an important role in the regulation of endothelial function. The inhibition of endothelial autophagy is associated with the reduced expression of protein disulfide isomerase 4 (PDIA-4); however, its role in endothelial cells is not known. Here, we report that endothelial cell-specific loss of PDIA-4 leads to impaired autophagic flux accompanied by loss of endothelial function and apoptosis. Endothelial cell-specific loss of PDIA-4 also induced marked changes in endothelial cell architecture, accompanied by the loss of endothelial markers and the gain of mesenchymal markers consistent with endothelial-to-mesenchymal transition (EndMT). The loss of PDIA-4 activated TGFβ-signaling, and inhibition of TGFβ-signaling suppressed EndMT in PDIA-4-silenced endothelial cells in vitro. Our findings help elucidate the role of PDIA-4 in endothelial autophagy and endothelial function and provide a potential target to modulate endothelial function and/or limit autophagy and EndMT in (patho-)physiological conditions. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Cardiovascular Diseases)
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Review

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23 pages, 2807 KiB  
Review
Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology
by Aman Singh, Kriti S. Bhatt, Hien C. Nguyen, Jefferson C. Frisbee and Krishna K. Singh
Int. J. Mol. Sci. 2024, 25(11), 6180; https://doi.org/10.3390/ijms25116180 - 4 Jun 2024
Cited by 1 | Viewed by 1836
Abstract
Under different pathophysiological conditions, endothelial cells lose endothelial phenotype and gain mesenchymal cell-like phenotype via a process known as endothelial-to-mesenchymal transition (EndMT). At the molecular level, endothelial cells lose the expression of endothelial cell-specific markers such as CD31/platelet-endothelial cell adhesion molecule, von Willebrand [...] Read more.
Under different pathophysiological conditions, endothelial cells lose endothelial phenotype and gain mesenchymal cell-like phenotype via a process known as endothelial-to-mesenchymal transition (EndMT). At the molecular level, endothelial cells lose the expression of endothelial cell-specific markers such as CD31/platelet-endothelial cell adhesion molecule, von Willebrand factor, and vascular-endothelial cadherin and gain the expression of mesenchymal cell markers such as α-smooth muscle actin, N-cadherin, vimentin, fibroblast specific protein-1, and collagens. EndMT is induced by numerous different pathways triggered and modulated by multiple different and often redundant mechanisms in a context-dependent manner depending on the pathophysiological status of the cell. EndMT plays an essential role in embryonic development, particularly in atrioventricular valve development; however, EndMT is also implicated in the pathogenesis of several genetically determined and acquired diseases, including malignant, cardiovascular, inflammatory, and fibrotic disorders. Among cardiovascular diseases, aberrant EndMT is reported in atherosclerosis, pulmonary hypertension, valvular disease, fibroelastosis, and cardiac fibrosis. Accordingly, understanding the mechanisms behind the cause and/or effect of EndMT to eventually target EndMT appears to be a promising strategy for treating aberrant EndMT-associated diseases. However, this approach is limited by a lack of precise functional and molecular pathways, causes and/or effects, and a lack of robust animal models and human data about EndMT in different diseases. Here, we review different mechanisms in EndMT and the role of EndMT in various cardiovascular diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Cardiovascular Diseases)
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20 pages, 3083 KiB  
Review
Neutrophil Extracellular Traps in Cardiovascular and Aortic Disease: A Narrative Review on Molecular Mechanisms and Therapeutic Targeting
by Nahla Ibrahim, Wolf Eilenberg, Christoph Neumayer and Christine Brostjan
Int. J. Mol. Sci. 2024, 25(7), 3983; https://doi.org/10.3390/ijms25073983 - 3 Apr 2024
Cited by 2 | Viewed by 2200
Abstract
Neutrophil extracellular traps (NETs), composed of DNA, histones, and antimicrobial proteins, are released by neutrophils in response to pathogens but are also recognized for their involvement in a range of pathological processes, including autoimmune diseases, cancer, and cardiovascular diseases. This review explores the [...] Read more.
Neutrophil extracellular traps (NETs), composed of DNA, histones, and antimicrobial proteins, are released by neutrophils in response to pathogens but are also recognized for their involvement in a range of pathological processes, including autoimmune diseases, cancer, and cardiovascular diseases. This review explores the intricate roles of NETs in different cardiovascular conditions such as thrombosis, atherosclerosis, myocardial infarction, COVID-19, and particularly in the pathogenesis of abdominal aortic aneurysms. We elucidate the mechanisms underlying NET formation and function, provide a foundational understanding of their biological significance, and highlight the contribution of NETs to inflammation, thrombosis, and tissue remodeling in vascular disease. Therapeutic strategies for preventing NET release are compared with approaches targeting components of formed NETs in cardiovascular disease. Current limitations and potential avenues for clinical translation of anti-NET treatments are discussed. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Cardiovascular Diseases)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Sodium-glucose transporter-2 inhibitors (SGLT2i) and myocardial ischemia: another good reason to consider these agents irrespective of diabetes?

Annunziata Nusca

Tentative Abstract: 
In recent years, introducing sodium-glucose transporter-2 inhibitors (SGLT2i) represented a turning point in treating cardiovascular diseases (CVD). Indeed, beyond their known effects on glycemic control and lipid profile, SGLT2i demonstrated clear benefits on cardiovascular morbidity and mortality, regardless of the presence of diabetes. These agents are currently recommended as first-line therapy in patients with heart failure, with reduced and preserved ejection fraction, to improve symptoms and reduce the risk of hospitalization. Although several studies showed how SGLT2i could reduce the incidence of major adverse cardiovascular events (MACEs), their real benefit on atherosclerosis progression and myocardial ischemia still needs to be fully understood. A global beneficial effect related to better glycemic and lipid control could be hypothesized. In this context, this narrative review summarizes the current knowledge regarding these novel anti-diabetic drugs in preventing and treating myocardial ischemia to define another possible field of utilization beyond glycemic control and heart failure.

 

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