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Biomedicines
Special Issues
Animal Models for the Study of Cardiovascular Physiology
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Animal Models for the Study of Cardiovascular Physiology

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

Deadline for manuscript submissions: closed (15 October 2024) | Viewed by 6895

Special Issue Editor

Dr. Sandra Lia Amaral

E-Mail Website
Guest Editor
1. Department of Physical Education, São Paulo State University-UNESP, Campus of Bauru, SP, Brazil
2. Joint Graduate Program in Physiological Sciences (PIPGCF), Federal University of Sao Carlos and São Paulo State University, UFSCar/UNESP, São Carlos, Brazil
Interests: hypertension; skeletal muscle; arterial stiffness; exercise training

Special Issue Information

Dear Colleagues,

Cardiovascular diseases, which include coronary heart disease, cerebrovascular disease, rheumatic heart disease, peripheral vascular disease, and other conditions, represent the leading cause of death worldwide. Among the top 10 diseases that lead the mortality rate worldwide, stroke and ischemic diseases are included here and are also consequences of hypertension. Since there are several behavioral risk factors for cardiovascular diseases, such as unhealthy diet, physical inactivity, tobacco consumption, and harmful use of alcohol, associated with hypertension, diabetes, and excess weight, the treatment for these pathologies can be very complex. Therefore, a deeper understanding of the disease mechanisms could significantly contribute to more effective treatment and to a reduction in premature deaths from cardiovascular diseases. Animal models are useful as they represent the main strategy for exploring the different mechanisms involved in cardiovascular diseases. Overall, this Special Issue invites you and your colleagues to share your expertise and knowledge by submitting original research articles, systematic reviews, and review articles that report new ideas and recent advances on this topic.

Dr. Sandra Lia Amaral
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

  • hypertension
  • stroke
  • myocardium infarction
  • arterial stiffness
  • supravalvular aortic stenosis
  • cardiac remodeling
  • capillary angiogenesis
  • exercise training
  • vascular diseases
  • non-pharmacological treatment

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Published Papers (6 papers)

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Research

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11 pages, 248 KiB  
Article
The Expression of Genes CYP1A1, CYP1B1, and CYP2J3 in Distinct Regions of the Heart and Its Possible Contribution to the Development of Hypertension
by Maria L. Perepechaeva, Natalia A. Stefanova, Alevtina Y. Grishanova and Nataliya G. Kolosova
Biomedicines 2024, 12(10), 2374; https://doi.org/10.3390/biomedicines12102374 - 17 Oct 2024
Viewed by 631
Abstract
Background: It is believed that alterations in the functioning of the cytochrome P450 (CYP), which participates in metabolic transformations of endogenous polyunsaturated fatty acids (PUFAs) (with the formation of cardioprotective or cardiotoxic products), affects the development of age-related cardiovascular diseases and reduces the [...] Read more.
Background: It is believed that alterations in the functioning of the cytochrome P450 (CYP), which participates in metabolic transformations of endogenous polyunsaturated fatty acids (PUFAs) (with the formation of cardioprotective or cardiotoxic products), affects the development of age-related cardiovascular diseases and reduces the effectiveness of some cardioselective drugs. For example, CYP2J2 activation or CYP1B1 inhibition protects against the cardiovascular toxicity of anticancer drugs. It is currently unclear whether CYPs capable of metabolizing arachidonic acid and ω-3 PUFAs to vasodilatory and vasoconstrictive derivatives are expressed in all heart regions. Methods: The work was performed on senescence-accelerated OXYS rats featuring elevated blood pressure, OXYSb rats (an OXYS substrain with normal blood pressure), and Wistar rats as a “healthy” control. The mRNA level was determined in the right and left ventricles, the right and left atria, and the aorta of 1-, 3-, and 12-month-old rats. Results: We showed that all heart regions express CYPs capable of metabolizing arachidonic acid and ω-3 PUFAs and revealed significant differences between heart regions both in the mRNA level of genes CYP1B1, CYP2J3, and CYP1A1 and in the time course of expression changes with age. Conclusions: We noticed that expression levels of these CYPs in the heart regions and aorta differ between hypertensive OXYS rats, normotensive OXYSb rats, and healthy Wistar rats but could not detect any clear-cut patterns associated with the hypertensive status of OXYS rats. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
15 pages, 663 KiB  
Article
Beta-Blockers of Different Generations: Features of Influence on the Disturbances of Myocardial Energy Metabolism in Doxorubicin-Induced Chronic Heart Failure in Rats
by Igor Belenichev, Olexiy Goncharov, Nina Bukhtiyarova, Oleh Kuchkovskyi, Victor Ryzhenko, Lyudmyla Makyeyeva, Valentyn Oksenych and Oleksandr Kamyshnyi
Biomedicines 2024, 12(9), 1957; https://doi.org/10.3390/biomedicines12091957 - 28 Aug 2024
Viewed by 1116
Abstract
Beta-blockers are first-line drugs in the treatment of chronic heart failure (CHF). However, there is no consensus on the specific effects of the beta-blockers of the I-III generation on energy metabolism in CHF. The aim of this study is to conduct a study [...] Read more.
Beta-blockers are first-line drugs in the treatment of chronic heart failure (CHF). However, there is no consensus on the specific effects of the beta-blockers of the I-III generation on energy metabolism in CHF. The aim of this study is to conduct a study of beta-blockers of different generations on myocardial energy metabolism in experimental CHF. CHF was modeled in white outbred rats by administering doxorubicin. The study drugs were administered intragastrically—new drug Hypertril (1-(β-phenylethyl)-4-amino-1,2,4-triazolium bromide)-3.5 mg/kg, Metoprolol—15 mg/kg, Nebivolol −10 mg/kg, Carvedilol 50 mg/kg, and Bisoprolol, 10 mg/kg. In the myocardium, the main indices of energy metabolism were determined—ATP, ADP, AMP, malate, lactate, pyruvate, succinate dehydrogenase (SDH) activity, and NAD-dependent malate dehydrogenase (NAD-MDH) activity. Traditional second-generation beta-blockers (Metoprolol and Bisoprolol) did not affect the studied indices of energy metabolism, and third-generation beta-blockers with additional properties—Carvedilol and, especially, Nebivalol and Hypertril—improved myocardial energy metabolism. The obtained results will help to expand our understanding of the effect of beta-blockers of various generations used to treat cardiovascular diseases on energy metabolism, and are also an experimental justification for the practical choice of these drugs in the complex therapy of CHF. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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13 pages, 3030 KiB  
Article
Loss of c-Kit in Endothelial Cells Protects against Hindlimb Ischemia
by Gustavo Falero-Diaz, Catarina de A. Barboza, Roberto I. Vazquez-Padron, Omaida C. Velazquez and Roberta M. Lassance-Soares
Biomedicines 2024, 12(6), 1358; https://doi.org/10.3390/biomedicines12061358 - 19 Jun 2024
Viewed by 895
Abstract
Background: Critical limb ischemia (CLI) is the end stage of peripheral artery disease (PAD), and around 30% of CLI patients are ineligible for current treatments. The angiogenic benefits of c-Kit have been reported in the ischemia scenario; however, the present study demonstrates the [...] Read more.
Background: Critical limb ischemia (CLI) is the end stage of peripheral artery disease (PAD), and around 30% of CLI patients are ineligible for current treatments. The angiogenic benefits of c-Kit have been reported in the ischemia scenario; however, the present study demonstrates the effects of specific endothelial c-Kit signaling in arteriogenesis during hindlimb ischemia. Methods: We created conditional knockout mouse models that decrease c-Kit (c-Kit VE-Cadherin CreERT2—c-Kit) or its ligand (SCF VE-Cadherin CreERT2—SCF) specifically in endothelial cells (ECs) after tamoxifen treatment. These mice and a control group (wild-type VE-Cadherin CreERT2—WT) were subjected to hindlimb ischemia or aortic crush to evaluate perfusion/arteriogenesis and endothelial barrier permeability, respectively. Results: Our data confirmed the lower gene expression of c-Kit and SCF in the ECs of c-Kit and SCF mice, respectively. In addition, we confirmed the lower percentage of ECs positive for c-Kit in c-Kit mice. Further, we found that c-Kit and SCF mice had better limb perfusion and arteriogenesis compared to WT mice. We also demonstrated that c-Kit and SCF mice had a preserved endothelial barrier after aortic crush compared to WT. Conclusions: Our data demonstrate the deleterious effects of endothelial SCF/c-Kit signaling on arteriogenesis and endothelial barrier integrity. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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14 pages, 3423 KiB  
Article
Pigs as Models to Test Cardiovascular Devices
by Yanina L. Rusakova, Denis S. Grankin, Kseniya S. Podolskaya and Irina Yu. Zhuravleva
Biomedicines 2024, 12(6), 1245; https://doi.org/10.3390/biomedicines12061245 - 3 Jun 2024
Viewed by 934
Abstract
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices [...] Read more.
Pigs as laboratory animals are used in preclinical studies aimed at developing medical devices for cardiac surgery. The anatomy of the cardiovascular system of these animals has been well studied and acknowledged as suitable for use and the testing of new cardiovascular devices developed for humans. However, there are no morphometric characteristics of the aortic root and thoraco-abdominal part of porcine aorta. This can lead to difficulties in experimental surgery and even result in the death of experimental animals due to the mismatch in the size of the implantable devices. Thus, such information is essential to enhance the efficiency of surgical technologies used for eliminating aortic pathologies in their various sections. The purpose of our research is to study the anatomy of the aorta in mini pigs and to assess whether the size, age, and sex of the animals affect the size of the main structures in their aortas. In addition, we attempted to compare the results obtained by transesophageal echocardiography (TEE) and angiography. We studied 28 laboratory mini pigs, dividing them into three groups by body weight (40–70 kg, 71–90 kg, and 90 kg). We did not find any relationship between the external somatometric characteristics of the animals and the size of their aortas. Animals have individual anatomical variability in their cardiovascular systems, which means that they need to be examined in terms of preoperative planning by any available method—echocardiography, angiography, or multispiral computed tomography (CT). Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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18 pages, 2035 KiB  
Article
Blockade of Inflammatory Markers Attenuates Cardiac Remodeling and Fibrosis in Rats with Supravalvular Aortic Stenosis
by Francine Duchatsch, Danyelle S. Miotto, Lidieli P. Tardelli, Thiago J. Dionísio, Dijon S. Campos, Carlos F. Santos, Katashi Okoshi and Sandra L. Amaral
Biomedicines 2023, 11(12), 3219; https://doi.org/10.3390/biomedicines11123219 - 5 Dec 2023
Viewed by 1181
Abstract
Since cardiac inflammation has been considered an important mechanism involved in heart failure, an anti-inflammatory treatment could control cardiac inflammation and mitigate the worsening of cardiac remodeling. This study evaluated the effects of dexamethasone (DEX) and ramipril treatment on inflammation and cardiac fibrosis [...] Read more.
Since cardiac inflammation has been considered an important mechanism involved in heart failure, an anti-inflammatory treatment could control cardiac inflammation and mitigate the worsening of cardiac remodeling. This study evaluated the effects of dexamethasone (DEX) and ramipril treatment on inflammation and cardiac fibrosis in an experimental model of heart failure induced by supravalvular aortic stenosis. Wistar rats (21d) were submitted to an aortic stenosis (AS) protocol. After 21 weeks, an echocardiogram and a maximal exercise test were performed, and after 24 weeks, rats were treated with DEX, ramipril or saline for 14d. The left ventricle (LV) was removed for histological and inflammatory marker analyses. The AS group showed exercise intolerance (−32% vs. Sham), higher relative wall thickness (+63%), collagen deposition and capillary rarefaction, followed by cardiac disfunction. Both treatments were effective in reducing cardiac inflammation, but only DEX attenuated the increased relative wall thickness (−17%) and only ramipril reduced LV fibrosis. In conclusion, both DEX and ramipril decreased cardiac inflammatory markers, which probably contributed to the reduced cardiac fibrosis and relative wall thickness; however, treated AS rats did not show any improvement in cardiac function. Despite the complex pharmacological treatment of heart failure, treatment with an anti-inflammatory could delay the patient’s poor prognosis. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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Review

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12 pages, 1545 KiB  
Review
The Monocrotaline Rat Model of Right Heart Disease Induced by Pulmonary Artery Hypertension
by Anna Maria Krstic, Timothy L. M. Jones, Amelia S. Power and Marie-Louise Ward
Biomedicines 2024, 12(9), 1944; https://doi.org/10.3390/biomedicines12091944 - 23 Aug 2024
Viewed by 1034
Abstract
Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right [...] Read more.
Pulmonary artery hypertension (PAH) is characterised by increased pulmonary vascular resistance (PVR) resulting in elevated pressure in the pulmonary artery supplying the pulmonary circulation. Disease of the right ventricle (RV) often manifests as a result of PAH placing excessive pressure on the right side of the heart. Although a relatively rare disease in humans, the impact of sustained PAH is severe, with poor outcomes even in treated individuals. As PAH develops, the blood flow is restricted through the pulmonary arteries and the right ventricle hypertrophies due to the increased strain of pumping blood through the pulmonary circulation. With time, RV hypertrophy progresses to right heart failure, impacting the supply of blood to the left ventricle and systemic circulation. Although right heart failure can currently be treated, it cannot be cured. There is therefore a need for more research into the physiological changes that cause the heart to fail under pressure overload. This review aims to evaluate the monocrotaline (MCT) rat model of PAH as a means of studying the cellular mechanisms associated with the development of RV hypertrophy and right heart failure. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology)
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