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Biomedicines
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Animal Models for the Study of Cardiovascular Physiology—Second Edition
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Animal Models for the Study of Cardiovascular Physiology—Second Edition

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 3084

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, 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 Issues, Collections and Topics in MDPI journals

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. Stroke and ischemic diseases are among the top 10 diseases regarding mortality rate worldwide, and these conditions are also consequences of hypertension. Since there are several behavioral risk factors for cardiovascular diseases, such as an unhealthy diet, physical inactivity, tobacco consumption, and the 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 of cardiovascular diseases could significantly contribute to more effective treatment and to a reduction in premature deaths from these 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 related to 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 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. 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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Related Special Issue

Published Papers (3 papers)

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Research

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16 pages, 1249 KB  
Article
Rosmarinic Acid Induces Vasorelaxation via Endothelium-Dependent, Potassium Channel-Related, and Calcium-Modulated Pathways: Evidence from Rat Aortic Rings
by Serdar Sahinturk and Naciye Isbil
Biomedicines 2025, 13(12), 2936; https://doi.org/10.3390/biomedicines13122936 - 29 Nov 2025
Viewed by 398
Abstract
Background: Hypertension and its complications are a major global health problem, and natural compounds with vasorelaxant effects are being investigated as potential antihypertensive agents. Objective: This study aimed to determine whether rosmarinic acid (RA) induces vasorelaxation in the rat thoracic aorta and to [...] Read more.
Background: Hypertension and its complications are a major global health problem, and natural compounds with vasorelaxant effects are being investigated as potential antihypertensive agents. Objective: This study aimed to determine whether rosmarinic acid (RA) induces vasorelaxation in the rat thoracic aorta and to elucidate the underlying mechanisms. Methods: Isolated thoracic aortic rings, with or without endothelium, were precontracted with phenylephrine and subsequently exposed to cumulative concentrations of RA. The roles of endothelium-derived factors, potassium channels, and calcium signaling were evaluated using selective pharmacological inhibitors and activators. In addition, the involvement of the AMPK pathway, adenylate cyclase/cAMP pathway, PKC signaling, β-adrenergic receptors, muscarinic receptors, and angiotensin II in RA-induced vasorelaxation was investigated. Results: RA induced a concentration-dependent vasorelaxation in endothelium-intact thoracic aortic rings (p < 0.001; pD2 = 7.67 ± 0.04). The vasorelaxant effect of RA was attenuated in endothelium-denuded vessels (pD2: 5.26 ± 0.18). The relaxation response was significantly attenuated by inhibitors of the PI3K/Akt/eNOS/NO/cGMP pathway and by blockers of BKCa, IKCa, and Kv potassium channels (p < 0.001). Furthermore, RA markedly inhibited both extracellular Ca2+ influx and intracellular Ca2+ release from the sarcoplasmic reticulum (p < 0.001). RA incubation also significantly reduced the contractions induced by angiotensin II (Ang II) and by the PKC activator PMA (p < 0.001). Other tested pathways had no significant influence on the vasorelaxant effect of RA (p > 0.05). Conclusions: These findings demonstrate that rosmarinic acid induces both endothelium-dependent and endothelium-independent vasorelaxation in the rat thoracic aorta through activation of the PI3K/Akt/eNOS/NO/cGMP pathway, opening of BKCa, IKCa, and Kv potassium channels, and suppression of Ca2+ mobilization. Additionally, inhibition of PKC- and angiotensin II-mediated vascular contraction contributes to RA-induced vasorelaxation. RA may therefore have therapeutic potential in the management of hypertension. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology—Second Edition)
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15 pages, 7582 KB  
Article
Novel Murine Model of Atherosclerosis Progression Induced by a Modified Paigen Diet
by María del Rosario Álvarez-Valadez, Alejandrina Rodríguez-Hernández, Felipa Andrade-Urzúa, Saraí Limón-Miranda, Adriana Ceballos-Gutiérrez, Jorge Agustín Velasco-Gutiérrez, Armando Gamboa-Domínguez, Adolfo Virgen-Ortiz and Enrique Sánchez-Pastor
Biomedicines 2025, 13(11), 2736; https://doi.org/10.3390/biomedicines13112736 - 8 Nov 2025
Viewed by 474
Abstract
Background/Objectives: To better understand the mechanisms involved in atherosclerosis, different models have been developed, but these fail when studying the progression of this disease. The purpose of this study was to standardize a new model of atherosclerosis progression in rats using Paigen-type [...] Read more.
Background/Objectives: To better understand the mechanisms involved in atherosclerosis, different models have been developed, but these fail when studying the progression of this disease. The purpose of this study was to standardize a new model of atherosclerosis progression in rats using Paigen-type modified atherogenic diet. Methods: The design included a control group (n = 16) and 64 rats with atherogenic Paigen-type diet subdivided into four subgroups with different doses (Athero 1, Athero 2, Athero 3, and Athero 4). The atherogenic diet was supplemented orally in sequential stages: 1) Hypervitaminic (1.5 mL/kg/day for 12 days) and 2) Hyperlipidic (48 days ad libitum). Blood pressure, heart rate, aortic histopathology, inflammatory biomarkers, and biochemical lipid and liver profiles were measured in all groups on days 30 and 60. Results: All Athero 1 rats were sacrificed due to a poisoning for vitamin D2 excess. Athero 2 rats were sacrificed at day 30 showing severe atherosclerotic lesions (grades V–VIII). Athero 3 rats showed mild lesions (I–IV) at day 30 and severe lesions (V–VIII) at day 60. Athero 4 rats showed mild lesions (I–IV) at days 30 and 60. Diet-dependent changes in blood pressure and heart rate were observed. Furthermore, glycemia, dyslipidemia, and liver profile were associated with the degree of atherosclerotic lesion. Conclusions: “Athero 3” atherogenic diet generates a stable model to study the progress of atherosclerosis in rats. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology—Second Edition)
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Review

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25 pages, 4280 KB  
Review
Deciphering the Enigma of Calcific Aortic Valve Disease: The Pivotal Role of Animal Models in Unraveling Pathogenesis and Advancing Therapeutic Strategies
by Pengning Fan, Yuqi Liu, Xingyu Qian, Fuqiang Tong, Yidan Zheng, Zhengfeng Fan, Ming Chen, Zhe Chen, Haoyang Zhai, Teng Zeng, Nianguo Dong, Fei Li, Xucong Shi and Li Xu
Biomedicines 2025, 13(10), 2369; https://doi.org/10.3390/biomedicines13102369 - 27 Sep 2025
Cited by 1 | Viewed by 1789
Abstract
Calcific aortic valve disease (CAVD) is a prevalent cardiovascular condition and is the most common heart valve disease globally. Hyperlipidemia and aging are key risk factors; consequently, with the aging global population, CAVD incidence continues to rise. Despite extensive research, the pathogenesis of [...] Read more.
Calcific aortic valve disease (CAVD) is a prevalent cardiovascular condition and is the most common heart valve disease globally. Hyperlipidemia and aging are key risk factors; consequently, with the aging global population, CAVD incidence continues to rise. Despite extensive research, the pathogenesis of CAVD remains unclear, leading to a lack of effective pharmacological therapies. Consequently, valve replacement surgery persists as the primary treatment option. Establishing suitable animal models is crucial for investigating the complex pathophysiological mechanisms of CAVD in vivo, although an optimal model has yet to be identified. This review provides a concise overview of CAVD pathogenesis and summarizes the application of common animal models—including mice, rats, rabbits, and pigs—in studying valve calcification. We specifically detail the construction of various models and their associated calcific aortic valve phenotypes. Furthermore, we outline common detection methods for assessing aortic valve calcification in these models and suggest future directions for developing improved animal models relevant to CAVD research. Full article
(This article belongs to the Special Issue Animal Models for the Study of Cardiovascular Physiology—Second Edition)
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