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Biomedicines
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Cellular Mechanisms of Cardiovascular Disease 2.0
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Cellular Mechanisms of Cardiovascular Disease 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 7806

Special Issue Editors

Dr. Tânia Martins-Marques

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Guest Editor
Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: cardiovascular biology; myocardial ischemia; heart failure; intercellular communication; gap junctions; extracellular vesicles; intracellular trafficking
Special Issues, Collections and Topics in MDPI journals
Dr. Gonçalo F. Coutinho

E-Mail Website
Guest Editor
Cardiothoracic Surgery Department, University Hospital and Centre of Coimbra, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: valvular heart disease; heart failure; coronary artery disease
Special Issues, Collections and Topics in MDPI journals
Dr. Attila Kiss

E-Mail Website
Guest Editor
Ludwig-Boltzmann Institute for Cardiovascular Research, Center for Biomedical Research and Translational Surgery, Medical University of Vienna, 1090 Vienna, Austria
Interests: vascular biology; pathophysiology of adverse cardiac remodeling; mechanism of myocardial ischemia and reperfusion injury; cardiomyopathies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD), particularly coronary artery disease (CAD) and stroke, remain the major cause of mortality and disability worldwide. Although cardiovascular outcomes have significantly improved due to early diagnosis and timely treatment, the prevalence of CVD is expected to increase in the coming years, highlighting the pressing need to identify novel biomarkers and disease-modifying treatments. In addition to classical risk factors, CVD burden is now recognized to be aggravated due to the growing population of cancer survivors treated with cardiotoxic cancer therapies or radiotherapy, which has fostered the development of a new field of research—cardio-oncology.

Across the spectrum of CVD, numerous cellular and molecular changes have been reported to occur in both myocytes and non-myocytes, leading to cardiac dysfunction. In fact, multiple molecular pathways converge in cardiac remodeling as well as aorta and mitral valve disease, including cardiomyocyte loss, extracellular matrix alterations, inflammation, oxidative stress, defective calcium homeostasis, intercellular communication, and metabolic abnormalities, which can be associated with a wide range of CVDs with distinct etiologies and clinical manifestations. Therefore, a major future challenge in cardiovascular medicine lies in understanding the molecular basis of cardiac and valvular remodeling, paving the way to the identification of more efficient diagnostic and therapeutic tools.

This Special Issue intends to bring together the latest findings in the field of cardiovascular biology and cardio-oncology, involving both cell-based studies and animal models of CVD aiming to identify novel mechanisms underlying cardiac remodeling and dysfunction.

Dr. Tânia Martins-Marques
Dr. Gonçalo F. Coutinho
Dr. Attila Kiss
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

  • inflammation
  • oxidative stress
  • intercellular communication
  • cardiac remodeling
  • atherosclerosis
  • aorta and mitral valve disease
  • myocardial infarction
  • cardiac hypertrophy
  • heart failure
  • cardio-oncology

Related Special Issue

Published Papers (6 papers)

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Research

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14 pages, 2435 KiB  
Article
Myocardial RNA Sequencing Reveals New Potential Therapeutic Targets in Heart Failure with Preserved Ejection Fraction
by José M. Inácio, Fernando Cristo, Miguel Pinheiro, Francisco Vasques-Nóvoa, Francisca Saraiva, Mafalda M. Nunes, Graça Rosas, Andreia Reis, Rita Coimbra, José Luís Oliveira, Gabriela Moura, Adelino Leite-Moreira and José António Belo
Biomedicines 2023, 11(8), 2131; https://doi.org/10.3390/biomedicines11082131 - 28 Jul 2023
Cited by 2 | Viewed by 1457
Abstract
Heart failure with preserved ejection fraction (HFpEF) represents a global health challenge, with limited therapies proven to enhance patient outcomes. This makes the elucidation of disease mechanisms and the identification of novel potential therapeutic targets a priority. Here, we performed RNA sequencing on [...] Read more.
Heart failure with preserved ejection fraction (HFpEF) represents a global health challenge, with limited therapies proven to enhance patient outcomes. This makes the elucidation of disease mechanisms and the identification of novel potential therapeutic targets a priority. Here, we performed RNA sequencing on ventricular myocardial biopsies from patients with HFpEF, prospecting to discover distinctive transcriptomic signatures. A total of 306 differentially expressed mRNAs (DEG) and 152 differentially expressed microRNAs (DEM) were identified and enriched in several biological processes involved in HF. Moreover, by integrating mRNA and microRNA expression data, we identified five potentially novel miRNA–mRNA relationships in HFpEF: the upregulated hsa-miR-25-3p, hsa-miR-26a-5p, and has-miR4429, targeting HAPLN1; and NPPB mRNA, targeted by hsa-miR-26a-5p and miR-140-3p. Exploring the predicted miRNA–mRNA interactions experimentally, we demonstrated that overexpression of the distinct miRNAs leads to the downregulation of their target genes. Interestingly, we also observed that microRNA signatures display a higher discriminative power to distinguish HFpEF sub-groups over mRNA signatures. Our results offer new mechanistic clues, which can potentially translate into new HFpEF therapies. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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10 pages, 436 KiB  
Communication
Prognostic Value of the Selected Polymorphisms in the CD36 Gene in the Domain-Encoding Lipid-Binding Region at a 10-Year Follow-Up for Early-Onset CAD Patients
by Michał Bartoszewicz and Monika Rać
Biomedicines 2023, 11(5), 1332; https://doi.org/10.3390/biomedicines11051332 - 30 Apr 2023
Viewed by 1063
Abstract
The polymorphism of the CD36 gene may have a decisive impact on the formation and progression of atherosclerotic changes. The aim of the study was to confirm the prognostic values of the previously studied polymorphisms in the CD36 gene within a 10-year follow-up [...] Read more.
The polymorphism of the CD36 gene may have a decisive impact on the formation and progression of atherosclerotic changes. The aim of the study was to confirm the prognostic values of the previously studied polymorphisms in the CD36 gene within a 10-year follow-up period. This is the first published report confirming the long-term observation of patients with CAD. The study group covered 100 early-onset CAD patients. It included 26 women not older than 55 years and 74 men not older than 50 years, tested in a ten-year study as a long-term follow-up after the first cardiovascular episode. There are no notable differences between the CD36 variants and the number of fatalities during observation, fatalities due to cardiological reasons, cases of myocardial infarction within a ten-year observation period, hospitalizations for cardiovascular issues, all cardiovascular occurrences, and the number of months lived. We have shown that the CD36 variants analyzed in this study do not appear to be related to the risk of early CAD occurrence in the Caucasian population in long-term observation. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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15 pages, 6267 KiB  
Article
Age-Dependent Changes in Calcium Regulation after Myocardial Ischemia–Reperfusion Injury
by Maria Bencurova, Terezia Lysikova, Katarina Leskova Majdova, Peter Kaplan, Peter Racay, Jan Lehotsky and Zuzana Tatarkova
Biomedicines 2023, 11(4), 1193; https://doi.org/10.3390/biomedicines11041193 - 17 Apr 2023
Viewed by 1171
Abstract
During aging, heart structure and function gradually deteriorate, which subsequently increases susceptibility to ischemia–reperfusion (IR). Maintenance of Ca2+ homeostasis is critical for cardiac contractility. We used Langendorff’s model to monitor the susceptibility of aging (6-, 15-, and 24-month-old) hearts to IR, with [...] Read more.
During aging, heart structure and function gradually deteriorate, which subsequently increases susceptibility to ischemia–reperfusion (IR). Maintenance of Ca2+ homeostasis is critical for cardiac contractility. We used Langendorff’s model to monitor the susceptibility of aging (6-, 15-, and 24-month-old) hearts to IR, with a specific focus on Ca2+-handling proteins. IR, but not aging itself, triggered left ventricular changes when the maximum rate of pressure development decreased in 24-month-olds, and the maximum rate of relaxation was most affected in 6-month-old hearts. Aging caused a deprivation of Ca2+-ATPase (SERCA2a), Na+/Ca2+ exchanger, mitochondrial Ca2+ uniporter, and ryanodine receptor contents. IR-induced damage to ryanodine receptor stimulates Ca2+ leakage in 6-month-old hearts and elevated phospholamban (PLN)-to-SERCA2a ratio can slow down Ca2+ reuptake seen at 2–5 μM Ca2+. Total and monomeric PLN mirrored the response of overexpressed SERCA2a after IR in 24-month-old hearts, resulting in stable Ca2+-ATPase activity. Upregulated PLN accelerated inhibition of Ca2+-ATPase activity at low free Ca2+ in 15-month-old after IR, and reduced SERCA2a content subsequently impairs the Ca2+-sequestering capacity. In conclusion, our study suggests that aging is associated with a significant decrease in the abundance and function of Ca2+-handling proteins. However, the IR-induced damage was not increased during aging. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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15 pages, 2066 KiB  
Article
Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction
by Mark B. Plotnikov, Galina A. Chernysheva, Vera I. Smol’yakova, Oleg I. Aliev, Tatyana I. Fomina, Lyubov A. Sandrikina, Irina V. Sukhodolo, Vera V. Ivanova, Anton N. Osipenko, Nina D. Anfinogenova, Andrei I. Khlebnikov, Dmitriy N. Atochin, Igor A. Schepetkin and Mark T. Quinn
Biomedicines 2023, 11(3), 714; https://doi.org/10.3390/biomedicines11030714 - 27 Feb 2023
Cited by 2 | Viewed by 1593
Abstract
Activation of c-Jun N-terminal kinases (JNKs) is involved in myocardial injury, left ventricular remodeling (LV), and heart failure (HF) after myocardial infarction (MI). The aim of this research was to evaluate the effects of a selective JNK inhibitor, 11H-indeno [1,2-b [...] Read more.
Activation of c-Jun N-terminal kinases (JNKs) is involved in myocardial injury, left ventricular remodeling (LV), and heart failure (HF) after myocardial infarction (MI). The aim of this research was to evaluate the effects of a selective JNK inhibitor, 11H-indeno [1,2-b]quinoxalin-11-one oxime (IQ-1), on myocardial injury and acute myocardial ischemia/reperfusion (I/R) in adult male Wistar rats. Intraperitoneal administration of IQ-1 (25 mg/kg daily for 5 days) resulted in a significant decrease in myocardial infarct size on day 5 after MI. On day 60 after MI, a significant (2.6-fold) decrease in LV scar size, a 2.2-fold decrease in the size of the LV cavity, a 2.9-fold decrease in the area of mature connective tissue, and a 1.7-fold decrease in connective tissue in the interventricular septum were observed compared with the control group. The improved contractile function of the heart resulted in a significant (33%) increase in stroke size, a 40% increase in cardiac output, a 12% increase in LV systolic pressure, a 28% increase in the LV maximum rate of pressure rise, a 45% increase in the LV maximum rate of pressure drop, a 29% increase in the contractility index, a 14% increase in aortic pressure, a 2.7-fold decrease in LV end-diastolic pressure, and a 4.2-fold decrease in LV minimum pressure. We conclude that IQ-1 has cardioprotective activity and reduces the severity of HF after MI. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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Review

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18 pages, 1436 KiB  
Review
Mechanisms of Myocardial Edema Development in CVD Pathophysiology
by Diana G. Kiseleva, Tatiana V. Kirichenko, Yuliya V. Markina, Vadim R. Cherednichenko, Ekaterina A. Gugueva and Alexander M. Markin
Biomedicines 2024, 12(2), 465; https://doi.org/10.3390/biomedicines12020465 - 19 Feb 2024
Viewed by 759
Abstract
Myocardial edema is the excess accumulation of fluid in the myocardial interstitium or cardiac cells that develops due to changes in capillary permeability, loss of glycocalyx charge, imbalance in lymphatic drainage, or a combination of these factors. Today it is believed that this [...] Read more.
Myocardial edema is the excess accumulation of fluid in the myocardial interstitium or cardiac cells that develops due to changes in capillary permeability, loss of glycocalyx charge, imbalance in lymphatic drainage, or a combination of these factors. Today it is believed that this condition is not only a complication of cardiovascular diseases, but in itself causes aggravation of the disease and increases the risks of adverse outcomes. The study of molecular, genetic, and mechanical changes in the myocardium during edema may contribute to the development of new approaches to the diagnosis and treatment of this condition. This review was conducted to describe the main mechanisms of myocardial edema development at the molecular and cellular levels and to identify promising targets for the regulation of this condition based on articles cited in Pubmed up to January 2024. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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18 pages, 576 KiB  
Review
Risk Factors and Cellular Differences in Heart Failure: The Key Role of Sex Hormones
by Elvira Delcuratolo, Alberto Palazzuoli, Francesca Coppi, Anna Vittoria Mattioli, Paolo Severino, Francesco Tramonte and Francesco Fedele
Biomedicines 2023, 11(11), 3052; https://doi.org/10.3390/biomedicines11113052 - 14 Nov 2023
Viewed by 888
Abstract
Patients with heart failure are conventionally stratified into phenotypic groups based on their ejection fraction. The aim of this stratification is to improve disease management with a more targeted therapeutic approach. A further subdivision based on patient gender is justified. It is recognized [...] Read more.
Patients with heart failure are conventionally stratified into phenotypic groups based on their ejection fraction. The aim of this stratification is to improve disease management with a more targeted therapeutic approach. A further subdivision based on patient gender is justified. It is recognized that women are underrepresented in randomized controlled clinical trials, resulting in limited clinical and molecular differentiation between males and females. However, many observational studies show that the onset, development, and clinical course of the disease may substantially differ between the two sexes. According to the emerging concept of precision medicine, investigators should further explore the mechanisms responsible for the onset of heart failure due to sex differences. Indeed, the synergistic or opposing effects of sex hormones on the cardiovascular system and underlying heart failure mechanisms have not yet been clarified. Sex hormones, risk factors impact, and cardiovascular adaptations may be relevant for a better understanding of the intrinsic pathophysiological mechanisms in the two sexes. Despite the differences, treatment for HF is similar across the whole population, regardless of sex and gender. In our review, we describe the main differences in terms of cardiovascular dysfunction, risk factors, and cellular signaling modifications related to the hormonal pattern. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiovascular Disease 2.0)
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