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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 1752

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 (3 papers)

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Research

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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://0-doi-org.brum.beds.ac.uk/10.3390/ijms25095025 - 4 May 2024
Viewed by 826
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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Review

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21 pages, 2528 KiB  
Review
Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review
by Antonio da Silva Menezes Junior, Ana Luísa Guedes de França-e-Silva, Henrique Lima de Oliveira, Khissya Beatryz Alves de Lima, Iane de Oliveira Pires Porto, Thays Millena Alves Pedroso, Daniela de Melo e Silva and Aguinaldo F. Freitas, Jr.
Int. J. Mol. Sci. 2024, 25(11), 5855; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25115855 - 28 May 2024
Viewed by 193
Abstract
Hypertrophic cardiomyopathy (HCM) is a heart condition characterized by cellular and metabolic dysfunction, with mitochondrial dysfunction playing a crucial role. Although the direct relationship between genetic mutations and mitochondrial dysfunction remains unclear, targeting mitochondrial dysfunction presents promising opportunities for treatment, as there are [...] Read more.
Hypertrophic cardiomyopathy (HCM) is a heart condition characterized by cellular and metabolic dysfunction, with mitochondrial dysfunction playing a crucial role. Although the direct relationship between genetic mutations and mitochondrial dysfunction remains unclear, targeting mitochondrial dysfunction presents promising opportunities for treatment, as there are currently no effective treatments available for HCM. This review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews guidelines. Searches were conducted in databases such as PubMed, Embase, and Scopus up to September 2023 using “MESH terms”. Bibliographic references from pertinent articles were also included. Hypertrophic cardiomyopathy (HCM) is influenced by ionic homeostasis, cardiac tissue remodeling, metabolic balance, genetic mutations, reactive oxygen species regulation, and mitochondrial dysfunction. The latter is a common factor regardless of the cause and is linked to intracellular calcium handling, energetic and oxidative stress, and HCM-induced hypertrophy. Hypertrophic cardiomyopathy treatments focus on symptom management and complication prevention. Targeted therapeutic approaches, such as improving mitochondrial bioenergetics, are being explored. This includes coenzyme Q and elamipretide therapies and metabolic strategies like therapeutic ketosis. Understanding the biomolecular, genetic, and mitochondrial mechanisms underlying HCM is crucial for developing new therapeutic modalities. Full article
(This article belongs to the Special Issue Molecular Pharmacology and Interventions in Cardiovascular Disease)
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15 pages, 748 KiB  
Review
Therapies for Cirrhotic Cardiomyopathy: Current Perspectives and Future Possibilities
by Hongqun Liu, Daegon Ryu, Sangyoun Hwang and Samuel S. Lee
Int. J. Mol. Sci. 2024, 25(11), 5849; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25115849 - 28 May 2024
Viewed by 193
Abstract
Cirrhotic cardiomyopathy (CCM) is defined as cardiac dysfunction associated with cirrhosis in the absence of pre-existing heart disease. CCM manifests as the enlargement of cardiac chambers, attenuated systolic and diastolic contractile responses to stress stimuli, and repolarization changes. CCM significantly contributes to mortality [...] Read more.
Cirrhotic cardiomyopathy (CCM) is defined as cardiac dysfunction associated with cirrhosis in the absence of pre-existing heart disease. CCM manifests as the enlargement of cardiac chambers, attenuated systolic and diastolic contractile responses to stress stimuli, and repolarization changes. CCM significantly contributes to mortality and morbidity in patients who undergo liver transplantation and contributes to the pathogenesis of hepatorenal syndrome/acute kidney injury. There is currently no specific treatment. The traditional management for non-cirrhotic cardiomyopathies, such as vasodilators or diuretics, is not applicable because an important feature of cirrhosis is decreased systemic vascular resistance; therefore, vasodilators further worsen the peripheral vasodilatation and hypotension. Long-term diuretic use may cause electrolyte imbalances and potentially renal injury. The heart of the cirrhotic patient is insensitive to cardiac glycosides. Therefore, these types of medications are not useful in patients with CCM. Exploring the therapeutic strategies of CCM is of the utmost importance. The present review summarizes the possible treatment of CCM. We detail the current status of non-selective beta-blockers (NSBBs) in the management of cirrhotic patients and discuss the controversies surrounding NSBBs in clinical practice. Other possible therapeutic agents include drugs with antioxidant, anti-inflammatory, and anti-apoptotic functions; such effects may have potential clinical application. These drugs currently are mainly based on animal studies and include statins, taurine, spermidine, galectin inhibitors, albumin, and direct antioxidants. We conclude with speculations on the future research directions in CCM treatment. Full article
(This article belongs to the Special Issue Molecular Pharmacology and Interventions in Cardiovascular Disease)
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