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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: 20 November 2025 | Viewed by 486

Special Issue Editor

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

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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 (1 paper)

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Research

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
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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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