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: 15 October 2024 | Viewed by 1358

Special Issue Editor


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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

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Keywords

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

Published Papers (1 paper)

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Research

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 837
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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