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Molecular Pathophysiology and Treatment of Coronary Artery Disease
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Molecular Pathophysiology and Treatment of Coronary Artery 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: closed (20 May 2026) | Viewed by 3606

Editor

Dr. Kazufumi Nakamura

E-Mail Website
Guest Editor
Center for Advanced Heart Failure, Okayama University Hospital, Okayama, Japan
Interests: cardiovascular system; cardiac sarcoidosis; coronary artery disease; vein anastomosis; dilated cardiomyopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Coronary artery disease (CAD) is a complex and heterogeneous condition. Etiologically based therapy is the best option. The molecular pathophysiology of CAD involves a combination of inflammatory processes, and lipid accumulation, which can lead to the progression of atherosclerosis, myocardial ischemia, and adverse cardiovascular events, including heart failure and sudden cardiac death. Despite significant advancements in understanding these mechanisms, the relative roles of genetic predisposition, environmental factors, and inflammatory pathways in disease initiation and progression remain subjects of ongoing debate.

This Special Issue is dedicated to the molecular pathophysiology and treatment of coronary artery-related diseases, including immune-related adverse events, coronary artery-related cardiovascular diseases. Research articles and reviews will inform you about recent developments and update the current stage of knowledge.

Dr. Kazufumi Nakamura
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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.

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Keywords

  • coronary artery disease
  • ischemic cardiomyopathy
  • immune-related adverse events
  • CAD associated with autoimmune diseases
  • coronary artery disease-related cardiomyopathy

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Published Papers (4 papers)

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Research

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13 pages, 873 KB  
Article
Regulation of Monocyte Perilipin-2 Expression in Acute and Chronic Coronary Syndromes: Pathogenetic Implications
by Francesco Canonico, Renzo Laborante, Chiara Pidone, Ramona Vinci, Mattia Galli, Eugenia Pisano, Alice Bonanni, Marianna Di Sario, Anna Severino, Lucia Lisi, Daniela Pedicino, Giovanna Liuzzo, Massimiliano Ruscica, Filippo Crea, Giuseppe Patti and Domenico D’Amario
Int. J. Mol. Sci. 2025, 26(19), 9550; https://doi.org/10.3390/ijms26199550 - 30 Sep 2025
Cited by 1 | Viewed by 1365
Abstract
PLIN2 is involved in the lipid metabolism of macrophages resident in atherosclerotic plaques, and its upregulation leads to lipid droplets (LDs) accumulation. LDs enlargement results in the macrophage transformation into foam cells, a key step for the onset of atherosclerosis. In the present [...] Read more.
PLIN2 is involved in the lipid metabolism of macrophages resident in atherosclerotic plaques, and its upregulation leads to lipid droplets (LDs) accumulation. LDs enlargement results in the macrophage transformation into foam cells, a key step for the onset of atherosclerosis. In the present study, we investigated the role of PLIN2 and its regulation mechanisms in atherosclerosis and plaque instability in patients with a diagnosis of ST-elevation myocardial infarction (STEMI) and chronic coronary syndrome (CCS). We enrolled STEMI (n = 122) and CCS patients (n = 45). Peripheral blood mononuclear cells were isolated from whole blood samples. The PLIN2 protein level was analyzed in CD14+ monocytes by flow cytometry. Lipidomic panel and proteasome activity were evaluated. PLIN2 protein expression was significantly correlated with the age of CAD patients. We found no significant difference in monocyte lipid content between the two patient groups. The PLIN2 increased in STEMI as compared to CCS patients (p < 0.001). The proteasome activity being higher in STEMI as compared to CCS patients (p < 0.001), significant inverse correlations were evident between PLIN2 levels and proteasome activity in the CCS groups (p = 0.02). PLIN2 expression was higher in STEMI as compared to CCS patients, suggesting an involvement in plaque instability. Despite the proteasome activity being higher in STEMI patients, probably due to the elevated inflammatory burden, PLIN2 could escape proteasome degradation in a more efficient manner in STEMI as compared to CCS patients. Full article
(This article belongs to the Special Issue Molecular Pathophysiology and Treatment of Coronary Artery Disease)
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14 pages, 2160 KB  
Article
Arthrospira Platensis Attenuates Endothelial Inflammation and Monocyte Activation
by Ilaria Leone, Valentino Costabile, Giovanni Smaldone, Monica Franzese, Andrea Soricelli and Anna D’Agostino
Int. J. Mol. Sci. 2025, 26(16), 7844; https://doi.org/10.3390/ijms26167844 - 14 Aug 2025
Cited by 1 | Viewed by 1266
Abstract
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality in industrialized countries. Coronary artery disease (CAD) represents the most prevalent form of cardiovascular disease and remains a leading cause of morbidity, mortality, and long-term disability worldwide. Therefore, the identification of early [...] Read more.
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality in industrialized countries. Coronary artery disease (CAD) represents the most prevalent form of cardiovascular disease and remains a leading cause of morbidity, mortality, and long-term disability worldwide. Therefore, the identification of early biomarkers and clarification of the mechanism of action of pharmacological adjuvants is urgently needed. Nutraceuticals such as Arthrospira platensis (commonly known as spirulina) have emerged as promising modulators for their notable vascular anti-inflammatory properties. In this study, we provide novel evidence of the anti-inflammatory and anti-atherosclerotic potential of Arthrospira platensis toward endothelial cells and immune interactions, combining in vitro assays with bioinformatic profiling. Spirulina treatment significantly attenuated endothelial and angiogenic activation, reducing pro-inflammatory cytokine and VEGFA/VEGFR2 expression. Additionally, it also decreased the activation and adhesion capabilities of THP-1 monocytic cell lines. Through computational analysis of the complex molecular mixture present in Arthrospira platensis, we have identified a subset of compounds exhibiting high structural similarity to CHEMBL3559503, a well-characterized synthetic molecule with dual activity as a TLR9 agonist and anti-angiogenic agent. This represents a novel insight, suggesting that spirulina may serve as a natural source of analogues capable of modulating both immune and angiogenic pathways. These results highlight Arthrospira platensis as a promising candidate nutraceutical for targeting endothelial/immune crosstalk in the context of atherosclerosis prevention, offering both mechanistic insights and translational potential. Full article
(This article belongs to the Special Issue Molecular Pathophysiology and Treatment of Coronary Artery Disease)
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Review

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23 pages, 1110 KB  
Review
Immunothrombotic Cell–Cell Communication Networks in Coronary Atherosclerosis: Critical Insights from Single-Cell and Spatial Systems Biology
by Beata Krasińska, Antoni Staniewski, Oliwia Kalus, Joanna Maćkowiak, Zofia Szymańska, Zofia Gramala, Katarzyna Zalewska, Michał Karpiński, Paulina Mertowska, Łucja Rolek, Kinga Koziarska, Krzysztof J. Filipiak, Mansur Rahnama, Mariusz Kowalewski, Calogera Pisano, Giuseppe Maria Raffa, Zbigniew Krasiński, Piotr Suwalski, Vincenzo Nuzzi, Ewelina Grywalska and Tomasz Urbanowiczadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2026, 27(13), 5900; https://doi.org/10.3390/ijms27135900 - 30 Jun 2026
Viewed by 83
Abstract
Coronary artery disease (CAD) is increasingly recognized as a thromboinflammatory disorder in which innate immune activation and coagulation are tightly coupled within the plaque microenvironment. Emerging single-cell and spatial technologies have refined this paradigm by demonstrating that these processes are not diffusely distributed [...] Read more.
Coronary artery disease (CAD) is increasingly recognized as a thromboinflammatory disorder in which innate immune activation and coagulation are tightly coupled within the plaque microenvironment. Emerging single-cell and spatial technologies have refined this paradigm by demonstrating that these processes are not diffusely distributed but instead concentrated within discrete cellular niches. This narrative review critically evaluates mechanistic and translational studies integrating single-cell RNA sequencing, spatial transcriptomics, and ligand–receptor modeling to characterize cell–cell communication networks driving immunothrombosis in CAD. Converging evidence from single-cell and spatial studies indicates substantial heterogeneity among macrophages, neutrophils, and smooth muscle cells, with functionally distinct subpopulations contributing differentially to inflammation, matrix remodeling, and thrombogenicity. Spatial analyses further demonstrate that procoagulant and inflammatory programs converge in anatomically defined high-risk regions, particularly at the plaque shoulder and sites of endothelial dysfunction. However, whether these transcriptional states represent causal drivers or epiphenomena remains unresolved. Many insights are derived from murine models or dissociated tissues, raising concerns regarding translational relevance and loss of spatial context. Additionally, computational inference of intercellular communication remains indirect and requires functional validation. In conclusion, immunothrombosis in CAD should be interpreted as an emergent property of spatially organized cellular networks rather than a uniform inflammatory state. While these approaches identify candidate therapeutic nodes, their clinical translation and the central challenge is to distinguish causal regulatory nodes from transcriptional correlates generated by high-dimensional profiling. Full article
(This article belongs to the Special Issue Molecular Pathophysiology and Treatment of Coronary Artery Disease)
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36 pages, 1750 KB  
Review
Istaroxime in Acute Heart Failure and Early Cardiogenic Shock: A Calcium-Cycling Approach to Inotropic Therapy
by Beata Krasińska, Giuseppe Maria Raffa, Calogera Pisano, Vincenzo Nuzzi, Paolo Manca, Krzysztof J. Filipiak, Mansur Rahnama, Anna Olasińska-Wiśniewska, Mariusz Kowalewski, Zbigniew Krasiński, Piotr Suwalski, Ewelina Grywalska and Tomasz Urbanowicz
Int. J. Mol. Sci. 2026, 27(13), 5779; https://doi.org/10.3390/ijms27135779 - 26 Jun 2026
Viewed by 218
Abstract
Acute heart failure (AHF) and cardiogenic shock (CS) remain major causes of cardiovascular morbidity, mortality, and healthcare utilization worldwide. Although inotropic agents are central to the management of low-output states, their clinical utility is fundamentally constrained by mechanisms that increase myocardial oxygen consumption, [...] Read more.
Acute heart failure (AHF) and cardiogenic shock (CS) remain major causes of cardiovascular morbidity, mortality, and healthcare utilization worldwide. Although inotropic agents are central to the management of low-output states, their clinical utility is fundamentally constrained by mechanisms that increase myocardial oxygen consumption, disrupt calcium homeostasis, and promote arrhythmogenesis, without improving long-term outcomes. These limitations reflect not only pharmacological shortcomings, but a broader conceptual reliance on amplification of intracellular calcium flux as the primary means of augmenting contractility. While effective in increasing cardiac output, this strategy imposes substantial energetic and electrophysiological costs and fails to address key abnormalities of the failing myocardium, including impaired calcium recirculation and diastolic dysfunction. Istaroxime is a first-in-class agent that combines Na+/K+-ATPase inhibition with enhancement of sarcoplasmic reticulum Ca2+-ATPase (sarcoplasmic reticulum Ca2+-ATPase isoform 2a (SERCA2a)) function, thereby modulating both calcium availability and reuptake. This dual mechanism promotes a more coordinated pattern of excitation–contraction coupling, integrating systolic augmentation with improved diastolic relaxation. Early clinical studies demonstrate a distinct hemodynamic profile characterized by increased stroke volume, preservation of heart rate, and stabilization or elevation of arterial pressure. These properties suggest a potential role for istaroxime in specific hemodynamic phenotypes, particularly hypotensive AHF and early cardiogenic shock, where conventional inotropes are limited by tachycardia or vasodilatory effects. However, current evidence is limited to phase II studies focused on hemodynamic endpoints, and the impact of istaroxime on survival, organ function, and disease progression remains unknown. Istaroxime represents a mechanistically distinct approach to inotropic therapy, shifting the paradigm from calcium amplification toward partial restoration of calcium cycling. Its clinical relevance will depend on whether this strategy can translate into improved patient outcomes—an objective that has thus far eluded the entire class of inotropic agents. Full article
(This article belongs to the Special Issue Molecular Pathophysiology and Treatment of Coronary Artery Disease)
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