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Molecular Pharmacology and Interventions in Cardiovascular Disease
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Molecular Pharmacology and Interventions in Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 853

Special Issue Editor

Dr. Magdalena Zabielska-Kaczorowska

E-Mail Website
Guest Editor
Department of Physiology, Medical University of Gdansk, 80-210 Gdansk, Poland
Interests: heart metabolism; purine metabolism; ischemic heart disease; cardioplegia; myocardial ischemia and infarction; cardiac energetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The prevalence of cardiovascular diseases, which are complex and multifunctional, rises as the mean age of the population increases. The size of the myocardial infarction remains a crucial therapeutic target, because it correlates with heart failure and mortality. Efforts are being directed towards the development of novel drugs via the physiochemical modification of drug molecules and the design and synthesis of new drugs, with an emphasis on drug delivery, controlled drug release, and the targeting of drugs to the site of action in order to enhance the therapeutic effect.

While numerous pre-clinical studies have revealed that certain pharmacologic agents and therapeutic maneuvers reduce the myocardial infarction size more significantly than reperfusion alone, very few of these therapies have translated into successful clinical trials or standard clinical application. The optimization of pharmacologic agents is critical to the development of diagnostic, treatment, and preventive strategies in the cardiology field. It is essential to promote the endogenous regeneration of the heart in order to improve the prognosis of patients with cardiac injury and to find effective therapeutic strategies for it.

This Special Issue focuses on the role of cardiovascular pharmacology and interventions in cardiac injury, aiming to elucidate pharmacologic strategies that may be employed to promote heart repair after cardiac injury.

Dr. Magdalena Zabielska-Kaczorowska
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 pharmacology
  • cardiovascular interventions
  • cardioprotection
  • myocardial ischemia and infarction
  • heart failure

Published Papers (1 paper)

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Research

12 pages, 1784 KiB  
Article
Investigation of Strategies to Block Downstream Effectors of AT1R-Mediated Signalling to Prevent Aneurysm Formation in Marfan Syndrome
by Irene Valdivia Callejon, Lucia Buccioli, Jarl Bastianen, Jolien Schippers, Aline Verstraeten, Ilse Luyckx, Silke Peeters, A. H. Jan Danser, Roland R. J. Van Kimmenade, Josephina Meester and Bart Loeys
Int. J. Mol. Sci. 2024, 25(9), 5025; https://doi.org/10.3390/ijms25095025 (registering DOI) - 04 May 2024
Viewed by 409
Abstract
Cardiovascular outcome in Marfan syndrome (MFS) patients most prominently depends on aortic aneurysm progression with subsequent aortic dissection. Angiotensin II receptor blockers (ARBs) prevent aneurysm formation in MFS mouse models. In patients, ARBs only slow down aortic dilation. Downstream signalling from the angiotensin [...] Read more.
Cardiovascular outcome in Marfan syndrome (MFS) patients most prominently depends on aortic aneurysm progression with subsequent aortic dissection. Angiotensin II receptor blockers (ARBs) prevent aneurysm formation in MFS mouse models. In patients, ARBs only slow down aortic dilation. Downstream signalling from the angiotensin II type 1 receptor (AT1R) is mediated by G proteins and β-arrestin recruitment. AT1R also interacts with the monocyte chemoattractant protein-1 (MCP-1) receptor, resulting in inflammation. In this study, we explore the targeting of β-arrestin signalling in MFS mice by administering TRV027. Furthermore, because high doses of the ARB losartan, which has been proven beneficial in MFS, cannot be achieved in humans, we investigate a potential additive effect by combining lower concentrations of losartan (25 mg/kg/day and 5 mg/kg/day) with barbadin, a β-arrestin blocker, and DMX20, a C-C chemokine receptor type 2 (CCR2) blocker. A high dose of losartan (50 mg/kg/day) slowed down aneurysm progression compared to untreated MFS mice (1.73 ± 0.12 vs. 1.96 ± 0.08 mm, p = 0.0033). TRV027, the combination of barbadin with losartan (25 mg/kg/day), and DMX-200 (90 mg/kg/day) with a low dose of losartan (5 mg/kg/day) did not show a significant beneficial effect. Our results confirm that while losartan effectively halts aneurysm formation in Fbn1C1041G/+ MFS mice, neither TRV027 alone nor any of the other compounds combined with lower doses of losartan demonstrate a notable impact on aneurysm advancement. It appears that complete blockade of AT1R function, achieved by administrating a high dosage of losartan, may be necessary for inhibiting aneurysm progression in MFS. Full article
(This article belongs to the Special Issue Molecular Pharmacology and Interventions in Cardiovascular Disease)
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