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Molecules at Play in Cardiovascular Diseases
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Molecules at Play in Cardiovascular Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 5423

Special Issue Editor

Prof. Dr. Dumitru A. Iacobas

E-Mail Website
Guest Editor
Personalized Genomics Laboratory, Undergraduate Medical Academy, Prairie View A&M University, Prairie View, TX 77446, USA
Interests: cancer therapy; cancer biomarker; neurogenomics; systems biology; intercellular communication; neurotransmission
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs), a large group of heart and blood vessel afflictions, are the leading causes of one in three deaths worldwide. Although CVDs have been intensively studied in humans and animal models, their underlying molecular bases are still not fully understood. It has now become clear that the circulatory system is a multidimensional mosaic of interacting, partially overlapping molecular processes, whose organizational principles are race/strain-, age, sex- and sex hormone-dependent and can be altered by diet, stress and other external stimuli. Moreover, the circulatory system directly interacts with all other systems of the human body, and, therefore, any CVD affects several organs.

In this Special Issue, we will provide the reader with updated experimental and theoretical developments that explore, analyze, and interpret data resulting from varied molecular studies. The contributing papers will present the remodeling of functional pathways at the molecular level in severe CVDs and their restoration following targeted therapies.

Prof. Dr. Dumitru A. Iacobas
Guest Editor

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Keywords

  • arrythmias
  • arteriosclerosis
  • congenital heart disease
  • coronary disease
  • diabetic cardiomyopathy
  • dilated cardiomyopathy
  • endocarditis
  • high blood pressure
  • hypertrophic cardiomyopathy
  • valvular heart diseases

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Published Papers (5 papers)

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Research

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27 pages, 4242 KB  
Article
Mitochondrial Collapse Responsible for Chagasic and Post-Ischemic Heart Failure Is Reversed by Cell Therapy Under Different Transcriptomic Topologies
by Dumitru A. Iacobas, Shavaiz Manzoor, Dennis Daniels, Sanda Iacobas and Lei Xi
Curr. Issues Mol. Biol. 2025, 47(11), 940; https://doi.org/10.3390/cimb47110940 - 12 Nov 2025
Cited by 1 | Viewed by 1225
Abstract
Although experimental evidence indicates that mitochondrial collapse is a common effect of both Chagas disease and post-ischemic heart failure and that cardiac anatomy and function are partially restored by stem cell therapy, the responsible molecular mechanisms are still under debate. Gene expression data [...] Read more.
Although experimental evidence indicates that mitochondrial collapse is a common effect of both Chagas disease and post-ischemic heart failure and that cardiac anatomy and function are partially restored by stem cell therapy, the responsible molecular mechanisms are still under debate. Gene expression data from our publicly accessible transcriptomic dataset obtained by profiling the left ventricle myocardia of mouse models of Chagas disease and post-ischemic heart failure were re-analyzed from the perspective of the Genomic Fabric Paradigm. In addition to the regulation of the gene expression levels, we determined the changes in the strength of the homeostatic control of transcript abundance and the remodeling of the gene networks responsible for the mitochondrial respiration. The analysis revealed that most of the mitochondrial genes assigned to the five complexes of the respiratory chain were significantly downregulated by both Chagas disease and ischemia but exhibited outstanding recovery of the normal expression levels following direct injection of bone-marrow-derived stem cells. However, instead of regaining the original expression control and gene networking, the treatment induced novel mitochondrial arrangements, suggesting that multiple transcriptomic topologies might be compatible with any given physiological or pathological state. This study confirmed several established mechanisms and identified novel gene expression signals, especially Cox4i2, Cox6b1, Cox7b, Ndufb11, and Tmem186, that warrant further investigations. Their broad rescue with cell therapy underscores mitochondria as a convergent, tractable target for cardiac repair. Full article
(This article belongs to the Special Issue Molecules at Play in Cardiovascular Diseases)
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12 pages, 4176 KB  
Article
Myocardium miRNA Analysis Reveals Potential Biomarkers of Sudden Coronary Death in Rats
by Chunmei Zhao, Xinyu Zhou, Yaqin Bai, Zhenxiang Zhao, Huaping Zhang, Cairong Gao, Keming Yun and Xiangjie Guo
Curr. Issues Mol. Biol. 2025, 47(11), 889; https://doi.org/10.3390/cimb47110889 - 28 Oct 2025
Viewed by 723
Abstract
This study aims to provide potential biomarkers and reveal the molecular mechanism of sudden coronary death (SCD). Rat models of atherosclerotic death (ASD), coronary atherosclerosis (AS), and acute myocardial ischemia (AMI) and sham groups were established via the gavage of high-fat emulsion and [...] Read more.
This study aims to provide potential biomarkers and reveal the molecular mechanism of sudden coronary death (SCD). Rat models of atherosclerotic death (ASD), coronary atherosclerosis (AS), and acute myocardial ischemia (AMI) and sham groups were established via the gavage of high-fat emulsion and left coronary artery ligation. The myocardium was collected, and transcriptome sequencing was performed. Differentially expressed miRNAs (DEmiRNAs) were identified using edeR software. The target genes were predicted using TargetScan, and functional enrichment analysis was performed via KEGG. Then, an miRNA–mRNA interaction network was constructed using Cytoscape. The key miRNAs with biomarker potential were identified using LASSO regression. A total of 217, 224, and 86 DEmiRNAs were identified in the ASD, AS, and AMI groups compared with the sham group, respectively. The Ras and Rap1 pathways were mainly expressed in ASD. The β-alanine and sphingolipid metabolisms were expressed in AMI. Finally, miR-106b, miR-195, miR-33, miR-652, miR-466b, and miR-6321 were identified as biomarkers of ASD. MiR-205, miR-877, miR-325, and miR-344b were identified as biomarkers of AMI. miR542-Atg12 was involved in the RIG-I-like receptor signaling pathway, miR6328-Gstz1 was involved in tyrosine metabolism, and miR483-Dusp5 was involved in the MAPK signaling pathway. This study provides a reference for the identification of SCD in forensic pathology. Full article
(This article belongs to the Special Issue Molecules at Play in Cardiovascular Diseases)
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15 pages, 13730 KB  
Article
IGFBP5 Promotes Atherosclerosis in APOE−/− Mice Through Phenotypic Transformation of VSMCs
by Aoqi Xiang, Hua Guan, Peihong Su, Lusha Zhang, Xiaochang Chen and Qi Yu
Curr. Issues Mol. Biol. 2025, 47(7), 555; https://doi.org/10.3390/cimb47070555 - 17 Jul 2025
Cited by 1 | Viewed by 1243
Abstract
Atherosclerosis constitutes a pathological process underlying cardiovascular diseases. There is growing evidence that IGFBP5 is a causative factor, although the conclusions of different studies are inconsistent. The present study aims to confirm the role and mechanism of IGFBP5 in atherosclerosis. The expression of [...] Read more.
Atherosclerosis constitutes a pathological process underlying cardiovascular diseases. There is growing evidence that IGFBP5 is a causative factor, although the conclusions of different studies are inconsistent. The present study aims to confirm the role and mechanism of IGFBP5 in atherosclerosis. The expression of IGFBP5 was induced in the skeletal muscle of male ApoE−/− mice, an atherosclerosis model, using adeno-associated virus, resulting in elevated circulating IGFBP5 levels. Changes in blood lipids were detected, and pathological changes in the aorta were observed. Analysis of IGFBP5 function using RNA sequencing and validation were performed in a mouse aortic smooth muscle cell line. The results demonstrated that IGFBP5 overexpression exacerbated the development of aortic lesions in this murine models without any discernible alterations in lipid profile parameters; the arterial transcriptomic landscape revealed that heightened IGFBP5 levels predominantly influenced pathways governing smooth muscle cell proliferation and motility. In vitro experimentation corroborated these findings, showcasing the stimulatory effect of IGFBP5 on VSMC (vascular smooth muscle cell) proliferation and migration, provoking a transition toward a proliferative phenotype. IGFBP5 promotes atherosclerosis in ApoE−/− mice through the phenotypic transformation of VSMCs. This finding suggests that IGFBP5 has the potential to serve as an indicator of atherosclerosis diagnosis and a target for therapeutic interventions in the future. Full article
(This article belongs to the Special Issue Molecules at Play in Cardiovascular Diseases)
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Review

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20 pages, 3356 KB  
Review
Neurocardiac Crosstalk: Sympathetic Remodeling and Arrhythmogenesis After Myocardial Infarction
by Tianshui Yu
Curr. Issues Mol. Biol. 2025, 47(12), 1037; https://doi.org/10.3390/cimb47121037 - 12 Dec 2025
Viewed by 1285
Abstract
Sympathetic remodeling following myocardial infarction (MI) is a critical mechanism underlying the development of malignant arrhythmias and sudden cardiac death (SCD). The cardiac sympathetic nervous system functions as a multi-level regulatory network, integrating centers from the cerebral cortex (e.g., the insular lobe and [...] Read more.
Sympathetic remodeling following myocardial infarction (MI) is a critical mechanism underlying the development of malignant arrhythmias and sudden cardiac death (SCD). The cardiac sympathetic nervous system functions as a multi-level regulatory network, integrating centers from the cerebral cortex (e.g., the insular lobe and anterior cingulate gyrus), subcortical structures (e.g., the paraventricular nucleus of the hypothalamus), and brainstem nuclei (e.g., the rostral ventrolateral medulla and nucleus of the solitary tract), down to the peripheral ganglia. Post-MI, this entire neural axis undergoes significant remodeling, which manifests as neuroinflammation in the central nervous system, alongside peripheral sympathetic nerve sprouting and heterogeneous hyperinnervation. This article provides a systematic review of the anatomical architecture of the cardiac sympathetic nerve and the regulatory mechanisms of sympathetic remodeling at various levels of the central nervous system after MI. It particularly focuses on key signaling pathways—including the TLR4/MyD88/NF-κB and P2X7R/NLRP3 inflammasome pathways, as well as GABAergic inhibition within the paraventricular nucleus—in addition to the peripheral remodeling mechanisms within the stellate ganglia. By synthesizing insights from these studies, this review offers a novel perspective for understanding the neuroimmune mechanisms of post-MI malignant arrhythmias and provides a theoretical foundation for elucidating the mechanisms of SCD in clinical practice. Full article
(This article belongs to the Special Issue Molecules at Play in Cardiovascular Diseases)
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Other

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12 pages, 255 KB  
Study Protocol
Seeking Novel Personalized and Sex-Specific Strategies for the Prevention and Treatment of Heart Failure Based on the Assessment of β1-Adrenergic Receptor Desensitization: The Contribution to the HEAL ITALIA Project
by Rosa Vona, Camilla Cittadini, Gianfranco Mattia, Rossella Puglisi, Barbara Ascione, Lucrezia Gambardella, Sonia Maccari, Giuseppe Marano and Paola Matarrese
Curr. Issues Mol. Biol. 2026, 48(2), 132; https://doi.org/10.3390/cimb48020132 - 25 Jan 2026
Viewed by 434
Abstract
Background: This study is part of the HEAL ITALIA partnership, funded by the National Recovery and Resilience Plan (PNRR) and the European Union. Heart failure (HF) is a serious health problem, with a reduced density of the β1-adrenergic receptor (β1-AR) in the myocardium [...] Read more.
Background: This study is part of the HEAL ITALIA partnership, funded by the National Recovery and Resilience Plan (PNRR) and the European Union. Heart failure (HF) is a serious health problem, with a reduced density of the β1-adrenergic receptor (β1-AR) in the myocardium as a hallmark. It is unclear whether this downregulation causes dysfunction or represents an epiphenomenon. Recent evidence implicates oxidative stress and mitochondrial signaling, particularly through the 18 kDa translocator protein (TSPO), in the regulation of the β1-AR, with possible modulation by estrogen. Objectives: To determine (1) the role of β1-AR desensitization in the onset and development of HF; (2) whether monocytes can represent a suitable ex vivo model for sex-oriented mechanistic studies in the cardiac field; (3) whether monocytes isolated from peripheral blood of patients can represent a diagnostic and/or therapy response biomarker by monitoring β1-AR density; (4) whether and how the mitochondrial receptor TSPO is involved in the β1-AR dysregulation observed in HF; and (5) whether the mechanisms linked to the onset of HF are regulated in a sex-specific manner through the effect of estrogen and/or the X chromosome on the expression of specific microRNAs. Methods: Using an integrated in vitro-ex vivo-in vivo methodological approach, we will evaluate the density of β1/β2-AR receptors, the downstream signaling (GRK2/β-arrestin), mitochondrial and redox parameters, and miRNA profiles in human monocytes and cardiomyocytes, and in mouse hearts after HF following pressure overload. Conclusions: The goal is to better understand the mechanisms underlying β1-AR desensitization, verify monocytes as peripheral markers of disease progression and response to therapy, and provide potentially useful information for the development of gender-specific therapies for heart failure. Full article
(This article belongs to the Special Issue Molecules at Play in Cardiovascular Diseases)
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