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Molecular Mechanisms and Therapeutic Targets in Cardiovascular Health and Cardiotoxicity
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Molecular Mechanisms and Therapeutic Targets in Cardiovascular Health and Cardiotoxicity

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: 20 May 2026 | Viewed by 1427

Special Issue Editor

Dr. Rui Vitorino

E-Mail Website
Guest Editor
Department of Medical Sciences, Institute of Biomedicine iBiMED, University of Aveiro, 3810-193 Aveiro, Portugal
Interests: proteomic; bioinformatic; body fluids; integrative analysis; pipelines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide, and the molecular underpinnings of these conditions are under active investigation. This Special Issue aims to provide a platform for high-quality original research and reviews focusing on the molecular mechanisms involved in cardiovascular physiology and pathophysiology, including ischemia, heart failure, arrhythmogenesis, myocardial remodeling, and endothelial dysfunction.

We particularly welcome studies elucidating the role of genes, non-coding RNAs, proteins, metabolites, oxidative stress, inflammation, and mitochondrial dynamics in cardiovascular health and disease. Another key area of focus is the molecular basis of cardiotoxicity induced by chemotherapeutic agents, environmental stressors, or novel therapeutic interventions.

This Special Issue invites contributions using molecular biology, biochemistry, pharmacology, and omics technologies to uncover new biomarkers, molecular pathways, and potential therapeutic targets in cardiology and cardio-oncology. Studies involving both in vitro and in vivo models, as well as translational approaches with molecular depth, are encouraged.

By assembling a collection of molecular-level investigations, this Special Issue will help advance our understanding of cardiovascular disease mechanisms and support the development of targeted interventions to improve clinical outcomes.

Dr. Rui Vitorino
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
  • ischemia, heart failure
  • arrhythmogenesis
  • myocardial remodeling
  • endothelial dysfunction
  • cardiology
  • cardio-oncology

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Published Papers (2 papers)

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13 pages, 1794 KB  
Article
Targeting Inflammation: Cytosporone B Modulates Imatinib-Driven Biochemical Alterations in Rat Heart
by Denise Börzsei, András Nagy, Viktória Kiss, Zoltán Virág, Gyöngyi Kis, Nikoletta Almási, Szilvia Török, Médea Veszelka, Csaba Varga and Renáta Szabó
Int. J. Mol. Sci. 2025, 26(20), 10018; https://doi.org/10.3390/ijms262010018 - 15 Oct 2025
Viewed by 311
Abstract
In recent decades, chemotherapy has significantly improved cancer survival, yet its adverse effects on non-cancerous tissues raise increasing concerns. In this context, growing attention has been focused on natural compounds that may be useful in mitigating the undesirable effects of chemotherapeutic agents. Here, [...] Read more.
In recent decades, chemotherapy has significantly improved cancer survival, yet its adverse effects on non-cancerous tissues raise increasing concerns. In this context, growing attention has been focused on natural compounds that may be useful in mitigating the undesirable effects of chemotherapeutic agents. Here, we aimed to demonstrate that Cytosporone B (CsnB) is a potent agent for counteracting the cardiovascular effects induced by Imatinib. To this end, 12-week-old male Wistar rats were studied; they were divided into three groups as follows: (1) control, (2) Imatinib-treated (Imatinib: 60 mg/kg/day, per os), (3) Imatinib + CsnB-treated (CsnB: 5 mg/kg/day, i.p.). After the two-week-long experimental period, rats were euthanized. Their hearts were used for the following biochemical measurements: NADPH oxidase (NOX4), high mobility group box 1 (HMGB1), peptidylarginine deiminase 4 (PAD4), inducible nitric oxide synthase (iNOS) expression, tumor necrosis factor-alpha (TNF-α) level, and myeloperoxidase (MPO) activity. Imatinib caused a marked upregulation of key inflammatory and oxidative markers, including HMGB1, TNF-α, MPO, iNOS, PAD4, and NOX4 in cardiac tissue; however, CsnB treatment mitigated these elevations, implying its role in opposing Imatinib-induced inflammatory and oxidative processes in the heart. Our findings suggest that CsnB holds promise as a cardioprotective agent capable of modulating Imatinib-induced adverse cardiac effects. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Cardiovascular Health and Cardiotoxicity)
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27 pages, 2791 KB  
Review
Key Signals Produced by Gut Microbiota Associated with Metabolic Syndrome, Cancer, Cardiovascular Diseases, and Brain Functions
by Leon M. T. Dicks
Int. J. Mol. Sci. 2025, 26(21), 10539; https://doi.org/10.3390/ijms262110539 - 29 Oct 2025
Viewed by 886
Abstract
Gut microbiota have a significant impact neurotransmitters, short-chain fatty acids (SCFAs), immune signaling molecules, and gut hormones. These signaling molecules interact with receptors on the gut wall, immune cells, or the enteric nervous system (ENS), and reach the central nervous system (CNS) via [...] Read more.
Gut microbiota have a significant impact neurotransmitters, short-chain fatty acids (SCFAs), immune signaling molecules, and gut hormones. These signaling molecules interact with receptors on the gut wall, immune cells, or the enteric nervous system (ENS), and reach the central nervous system (CNS) via the Vagus nerve (VN). SCFAs interact with G protein-coupled receptors (GPCRs), Toll-like receptors (TLRs), and proliferator-activated receptors (PPARs), influencing inflammatory reactions, gut motility, nutrient absorption, hormone secretion, neurochemical signaling, and brain functions. Olfactory receptor OR51E1 influences blood pressure, vascular reactivity, and arterial stiffness. Activation of the brainstem nucleus tractus solitarius (NTS) by glucagon-like peptide 1 (GLP-1) influences mood, cognition, and gastrointestinal motility. Prolactin-releasing peptide (PrRP) binds to its receptor (PrRPR), suppressing food intake, and regulating stress, cardiovascular reactions, and circadian rhythms. In-depth studies on how gut microbiota control cognitive behavior, mood, and neuropsychiatric disorders are lacking. G protein receptor 119 (GPR119) suppresses appetite and may find an application in the treatment of type 2 diabetes and obesity. The binding of butyrate to nuclear factor kappa B (NF-κB) and proliferator-activated receptor γ (PPARγ) regulates the production of pro-and anti-inflammatory cytokines. This suppresses protein CD36, preventing the uptake of oxidized low-density lipoprotein (ox-LDL) and cardiovascular diseases (CVDs). This review focuses on a few prominent health conditions related to CVDs, i.e., metabolic syndrome (MetS), cancer, and brain functions. Information in this review is based on animal and preclinical studies published in repositories such as PubMed, the National Institutes of Health (NIH), NIH PubChem, ScienceDirect, MDPI, Frontiers, Cell Press, and the CAS Content Collection. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Cardiovascular Health and Cardiotoxicity)
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