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Biomedicines
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In Vitro Models of Cardiovascular Diseases and Toxicity
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In Vitro Models of Cardiovascular Diseases and Toxicity

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 March 2025) | Viewed by 10365

Special Issue Editor

Dr. Federico Vozzi

E-Mail Website
Guest Editor
Institute of Clinical Physiology, National Research Council (CNR), 56124 Pisa, Italy
Interests: cardiovascular diseases, tissue engineering, biomaterials, in vitro cell culture, new approach methodologies

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are the leading cause of morbidity and mortality and a substantial economic burden on the healthcare system globally. Several factors participate in their development: some more established and studied (smoking, diabetes, hypercholesterolemia, genetics), others external, come to the fore more recently (pollution, chemical compounds, etc.). Cardiovascular diseases and evaluation of toxicity share a series of mechanisms at the cell level, presenting a quite level of complexity to study in humans or animals.

The use of in vitro systems could help obtain specific information on cellular responses, favoring the study of the pathophysiology of diseases as well as evaluating the effects on the cell biology of several chemical compounds. In particular, in vitro models, which take methodologies at the interface of different specialties (e.g., biology, genetics, bioengineering, bioinformatics, physics), could provide a more reliable and close-to-reality response to researchers.

This Special Issue will focus on the cardiovascular in vitro models to mimic and study the pathophysiology associated with cardiovascular diseases and/or toxicity of compounds (i.e., pharmaceutical drugs, industrial chemicals, environmental toxicants) and their advantages and limitations, based on different approaches as:

  • 3D models
  • Biomaterials
  • Bioreactor
  • Microsystems
  • New approach methodologies
  • Co-cultures
  • Engineered cellular systems
  • Data integration with in silico models

Dr. Federico Vozzi
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. 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

  • cardiovascular diseases
  • tissue engineering
  • organ-on-chip
  • 3D systems
  • co-cultures
  • toxicity

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Published Papers (4 papers)

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Research

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14 pages, 13188 KiB  
Article
Ultrastructural and Molecular Analysis of Vascular Smooth Muscle Cells During the Switch from a Physiological to a Pathological Phenotype
by Elisa Persiani, Elisa Ceccherini, Alessandra Falleni, Ilaria Gisone, Chiara Ippolito, Letizia Mattii, Antonella Cecchettini and Federico Vozzi
Biomedicines 2025, 13(5), 1127; https://doi.org/10.3390/biomedicines13051127 - 6 May 2025
Viewed by 230
Abstract
Background/Objectives: Under physiological conditions, vascular smooth muscle cells (VSMCs) are in a quiescent contractile state, but under pathological conditions, such as atherosclerosis, they change their phenotype to synthetic, characterized by increased proliferation, migration, and production of an extracellular matrix. Furthermore, VSMCs can [...] Read more.
Background/Objectives: Under physiological conditions, vascular smooth muscle cells (VSMCs) are in a quiescent contractile state, but under pathological conditions, such as atherosclerosis, they change their phenotype to synthetic, characterized by increased proliferation, migration, and production of an extracellular matrix. Furthermore, VSMCs can undergo calcification, switching to an osteoblast-like phenotype, contributing to plaque instability. Methods: In this study, we analyzed the phenotypic changes in VSMCs during the transition from a physiological to a pathological state, a key process in the progression of atherosclerosis, using confocal and transmission electron microscopy, real-time PCR, and intracellular calcium quantification. Results: Confocal and transmission electron microscopy revealed a prominent remodeling of the actin cytoskeleton, increasing autophagic vacuoles in synthetic VSMCs and the deposition of calcium microcrystals in calcified cells. Immunofluorescence analysis revealed differential expression of α-SMA (contractile marker) and galectin-3 (synthetic marker), confirming the phenotypic changes. Real-time PCR further validated these changes, showing upregulation of RUNX-2, a marker of osteogenic transition, in calcified VSMCs. Conclusions: This study highlights the dynamic plasticity of VSMCs and their role in atherosclerosis progression. Understanding the characteristics of these phenotypic transitions can help develop targeted therapies to mitigate vascular calcification and plaque instability, potentially countering cardiovascular disease. Full article
(This article belongs to the Special Issue In Vitro Models of Cardiovascular Diseases and Toxicity)
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23 pages, 12660 KiB  
Article
Optimizing Cardiomyocyte Differentiation: Comparative Analysis of Bone Marrow and Adipose-Derived Mesenchymal Stem Cells in Rats Using 5-Azacytidine and Low-Dose FGF and IGF Treatment
by Ahmed Farag, Sai Koung Ngeun, Masahiro Kaneda, Mohamed Aboubakr and Ryou Tanaka
Biomedicines 2024, 12(8), 1923; https://doi.org/10.3390/biomedicines12081923 - 22 Aug 2024
Cited by 5 | Viewed by 1931
Abstract
Mesenchymal stem cells (MSCs) exhibit multipotency, self-renewal, and immune-modulatory properties, making them promising in regenerative medicine, particularly in cardiovascular treatments. However, optimizing the MSC source and induction method of cardiac differentiation is challenging. This study compares the cardiomyogenic potential of bone marrow (BM)-MSCs [...] Read more.
Mesenchymal stem cells (MSCs) exhibit multipotency, self-renewal, and immune-modulatory properties, making them promising in regenerative medicine, particularly in cardiovascular treatments. However, optimizing the MSC source and induction method of cardiac differentiation is challenging. This study compares the cardiomyogenic potential of bone marrow (BM)-MSCs and adipose-derived (AD)-MSCs using 5-Azacytidine (5-Aza) alone or combined with low doses of Fibroblast Growth Factor (FGF) and Insulin-like Growth Factor (IGF). BM-MSCs and AD-MSCs were differentiated using two protocols: 10 μmol 5-Aza alone and 10 μmol 5-Aza with 1 ng/mL FGF and 10 ng/mL IGF. Morphological, transcriptional, and translational analyses, along with cell viability assessments, were performed. Both the MSC types exhibited similar morphological changes; however, AD-MSCs achieved 70–80% confluence faster than BM-MSCs. Surface marker profiling confirmed CD29 and CD90 positivity and CD45 negativity. The differentiation protocols led to cell flattening and myotube formation, with earlier differentiation in AD-MSCs. The combined protocol reduced cell mortality in BM-MSCs and enhanced the expression of cardiac markers (MEF2c, Troponin I, GSK-3β), particularly in BM-MSCs. Immunofluorescence confirmed cardiac-specific protein expression in all the treated groups. Both MSC types exhibited the expression of cardiac-specific markers indicative of cardiomyogenic differentiation, with the combined treatment showing superior efficiency for BM-MSCs. Full article
(This article belongs to the Special Issue In Vitro Models of Cardiovascular Diseases and Toxicity)
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15 pages, 1729 KiB  
Article
Differential Mitochondrial Bioenergetics in Neurons and Astrocytes Following Ischemia-Reperfusion Injury and Hypothermia
by Santiago J. Miyara, Koichiro Shinozaki, Kei Hayashida, Muhammad Shoaib, Rishabh C. Choudhary, Stefanos Zafeiropoulos, Sara Guevara, Junhwan Kim, Ernesto P. Molmenti, Bruce T. Volpe and Lance B. Becker
Biomedicines 2024, 12(8), 1705; https://doi.org/10.3390/biomedicines12081705 - 1 Aug 2024
Cited by 1 | Viewed by 3006
Abstract
The close interaction between neurons and astrocytes has been extensively studied. However, the specific behavior of these cells after ischemia-reperfusion injury and hypothermia remains poorly characterized. A growing body of evidence suggests that mitochondria function and putative transference between neurons and astrocytes may [...] Read more.
The close interaction between neurons and astrocytes has been extensively studied. However, the specific behavior of these cells after ischemia-reperfusion injury and hypothermia remains poorly characterized. A growing body of evidence suggests that mitochondria function and putative transference between neurons and astrocytes may play a fundamental role in adaptive and homeostatic responses after systemic insults such as cardiac arrest, which highlights the importance of a better understanding of how neurons and astrocytes behave individually in these settings. Brain injury is one of the most important challenges in post-cardiac arrest syndrome, and therapeutic hypothermia remains the single, gold standard treatment for neuroprotection after cardiac arrest. In our study, we modeled ischemia-reperfusion injury by using in vitro enhanced oxygen-glucose deprivation and reperfusion (eOGD-R) and subsequent hypothermia (HPT) (31.5 °C) to cell lines of neurons (HT-22) and astrocytes (C8-D1A) with/without hypothermia. Using cell lysis (LDH; lactate dehydrogenase) as a measure of membrane integrity and cell viability, we found that neurons were more susceptible to eOGD-R when compared with astrocytes. However, they benefited significantly from HPT, while the HPT effect after eOGD-R on astrocytes was negligible. Similarly, eOGD-R caused a more significant reduction in adenosine triphosphate (ATP) in neurons than astrocytes, and the ATP-enhancing effects from HPT were more prominent in neurons than astrocytes. In both neurons and astrocytes, measurement of reactive oxygen species (ROS) revealed higher ROS output following eOGD-R, with a non-significant trend of differential reduction observed in neurons. HPT after eOGD-R effectively downregulated ROS in both cells; however, the effect was significantly more effective in neurons. Lipid peroxidation was higher after eOGD-R in neurons, while in astrocytes, the increase was not statistically significant. Interestingly, HPT had similar effects on the reduction in lipoperoxidation after eOGD-R with both types of cells. While glutathione (GSH) levels were downregulated after eOGD-R in both cells, HPT enhanced GSH in astrocytes, but worsened GSH in neurons. In conclusion, neuron and astrocyte cultures respond differently to eOGD-R and eOGD-R + HTP treatments. Neurons showed higher sensitivity to ischemia-reperfusion insults than astrocytes; however, they benefited more from HPT therapy. These data suggest that given the differential effects from HPT in neurons and astrocytes, future therapeutic developments could potentially enhance HPT outcomes by means of neuronal and astrocytic targeted therapies. Full article
(This article belongs to the Special Issue In Vitro Models of Cardiovascular Diseases and Toxicity)
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Review

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15 pages, 601 KiB  
Review
In Vitro Models of Cardiovascular Calcification
by Andrea Tóth, Enikő Balogh and Viktória Jeney
Biomedicines 2024, 12(9), 2155; https://doi.org/10.3390/biomedicines12092155 - 23 Sep 2024
Cited by 3 | Viewed by 2090
Abstract
Cardiovascular calcification, characterized by hydroxyapatite deposition in the arterial wall and heart valves, is associated with high cardiovascular morbidity and mortality. Cardiovascular calcification is a hallmark of aging but is frequently seen in association with chronic diseases, such as chronic kidney disease (CKD), [...] Read more.
Cardiovascular calcification, characterized by hydroxyapatite deposition in the arterial wall and heart valves, is associated with high cardiovascular morbidity and mortality. Cardiovascular calcification is a hallmark of aging but is frequently seen in association with chronic diseases, such as chronic kidney disease (CKD), diabetes, dyslipidemia, and hypertension in the younger population as well. Currently, there is no therapeutic approach to prevent or cure cardiovascular calcification. The pathophysiology of cardiovascular calcification is highly complex and involves osteogenic differentiation of various cell types of the cardiovascular system, such as vascular smooth muscle cells and valve interstitial cells. In vitro cellular and ex vivo tissue culture models are simple and useful tools in cardiovascular calcification research. These models contributed largely to the discoveries of the numerous calcification inducers, inhibitors, and molecular mechanisms. In this review, we provide an overview of the in vitro cell culture and the ex vivo tissue culture models applied in the research of cardiovascular calcification. Full article
(This article belongs to the Special Issue In Vitro Models of Cardiovascular Diseases and Toxicity)
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