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Biomedicines
Special Issues
Coronary Artery Disease: Current Evidence and Future Perspectives
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Coronary Artery Disease: Current Evidence and Future Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 599

Special Issue Editor

Prof. Dr. Tadateru Takayama

E-Mail Website
Guest Editor
Division of General Medicine, Department of Internal Medicine, Nihon University School of Medicine, 30-1 Oyaguchikamicho, Itabashi, Tokyo 173-8610, Japan
Interests: lipid metabolism; residual cardiovascular risk; small dense LDL; lipoprotein(a); endothelial dysfunction; oxidative stress; inflammation; coronary artery disease

Special Issue Information

Dear Colleagues,

Despite major advances in lipid-lowering therapy, coronary artery disease (CAD) continues to pose a substantial clinical burden. Accumulating evidence suggests that residual cardiovascular risk persists even after achieving guideline-recommended LDL-C levels, highlighting the importance of addressing other contributors such as small dense LDL, lipoprotein(a), endothelial dysfunction, and oxidative stress. This Special Issue aims to explore the current understanding and future directions in the management of CAD, with a particular focus on mechanisms beyond traditional lipid metrics. We welcome original research and comprehensive reviews covering novel biomarkers, lipid subfractions, vascular function, inflammation, and emerging therapeutic strategies for residual risk reduction in CAD.

Prof. Dr. Tadateru Takayama
Guest Editor

Manuscript Submission Information

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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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • coronary artery disease
  • lipid-lowering therapy
  • residual risk
  • small dense LDL
  • lipoprotein(a)
  • endothelial dysfunction
  • oxidative stress
  • inflammation
  • biomarkers
  • cardiovascular prevention

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Published Papers (1 paper)

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Research

24 pages, 2759 KB  
Article
Factors Released by Polarized Neutrophil-like Cells Modulate Cardiac Fibroblast Phenotype and Limit the Inflammatory Response After Myocardial Infarction
by Letitia Ciortan, Ana-Maria Gan, Sergiu Cecoltan, Mihaela Serbanescu, Andreea Cristina Mihaila, Razvan Daniel Macarie, Monica Madalina Tucureanu, Miruna Larisa Naie, Mihai Bogdan Preda, Bogdan-Paul Cosman, Galyna Bila, Rostyslav Bilyy and Elena Butoi
Biomedicines 2025, 13(11), 2829; https://doi.org/10.3390/biomedicines13112829 - 20 Nov 2025
Viewed by 347
Abstract
Background: Following myocardial infarction (MI), cardiac fibroblasts (CFs) adopt distinct phenotypes to ensure scar formation and healing. Although leukocytes are a critical driver of post-MI healing, the role of neutrophils in modulating CF phenotype remains insufficiently explored. We therefore investigated the impact [...] Read more.
Background: Following myocardial infarction (MI), cardiac fibroblasts (CFs) adopt distinct phenotypes to ensure scar formation and healing. Although leukocytes are a critical driver of post-MI healing, the role of neutrophils in modulating CF phenotype remains insufficiently explored. We therefore investigated the impact of soluble mediators released by neutrophil subtypes found post-MI—pro-inflammatory (N1) and anti-inflammatory (N2)—on shaping CFs phenotype. Methods: In vitro, human 3D grown CFs were indirectly co-cultured with N1 or N2 neutrophil-like cells using a two-chamber Transwell system. After 24 h, expression of inflammatory, remodeling, and pro-fibrotic markers was evaluated in fibroblasts and conditioned media. In vivo, soluble mediators derived from polarized mouse neutrophils (SN1 or SN2) were injected into the infarcted myocardium of C57BL/6J after MI surgery. The effects on the healing process were investigated at 1 and 7 days post-MI. Results: In vitro, CFs were found to exhibit a pro-inflammatory and matrix-degrading phenotype following indirect co-culture with N1 cells, characterized by overexpression of IL-1β, IL-6, MCP-1, and metalloproteases MMP-3/MMP-9. In vivo, both SN1 and SN2 treatments significantly reduced pro-inflammatory markers IL-1β and IL-6 gene expression at day 1 post-MI (inflammatory phase). At day 7 post-MI (resolution phase), SN1/SN2 treatments continued to limit local inflammation, while mitigating fibrotic remodeling by reducing CCN2, α-SMA, and key extracellular matrix proteins. Conclusions: Together, these findings suggest that while N1-derived mediators promote a pro-inflammatory fibroblast phenotype in vitro, factors secreted by both N1 and N2 support a more balanced reparative response in vivo, by limiting local inflammation and potentially mitigating adverse remodeling post-MI. Full article
(This article belongs to the Special Issue Coronary Artery Disease: Current Evidence and Future Perspectives)
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