Ischemic Heart Disease: From Cellular Level to Clinical Approaches

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 25 March 2026 | Viewed by 680

Special Issue Editors


E-Mail Website
Guest Editor
Clinic for Cardiology, University Clinical Center of Serbia, Belgrade, Serbia
Interests: ischaemic heart disease; PCI; chronic total occlusion

E-Mail Website
Guest Editor
1. Cardiovascular Institute Dedinje, Belgrade, Serbia
2. Faculty of Medicine, University of Belgrade, Belgrade, Serbia
Interests: ischaemic heart disease; PCI; chronic total occlusion

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this upcoming Special Issue, entitled “Ischemic Heart Disease: From Cellular Level to Clinical Approaches.”

Ischemic heart disease (IHD) remains a leading cause of morbidity and mortality worldwide, with a complex pathophysiology rooted in molecular and cellular dysfunction. This Special Issue will highlight cutting-edge research that explores the fundamental mechanisms underlying IHD and its clinical manifestations—from classic myocardial ischemia and reperfusion injury to inflammation, chronic remodeling, and fibrosis.

We particularly welcome studies focusing on oxidative stress, mitochondrial dysfunction, inflammatory signaling, endothelial biology, and cardiomyocyte death pathways. Emerging areas such as epigenetic regulation, non-coding RNAs, immunometabolism, and single-cell transcriptomics are of particular interest, as they offer new therapeutic insights and precision medicine opportunities.

Additionally, we encourage contributions exploring mechanisms of angiogenesis, ischemic preconditioning, and advanced nanotechnology-based drug delivery systems. Both original research articles and reviews are welcome, provided that they offer strong molecular or cellular insights relevant to the pathogenesis, diagnosis, or treatment of ischemic heart disease.

By integrating diverse experimental approaches, this Special Issue will deepen our understanding of IHD and accelerate the development of targeted interventions.

We look forward to receiving your valuable contributions.

Dr. Stefan A. Juričić
Dr. Milan R. Dobrić
Guest Editors

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • ischemic heart disease
  • myocardial ischemia
  • reperfusion injury
  • oxidative stress
  • mitochondrial dysfunction
  • cardiomyocyte death
  • endothelial dysfunction
  • inflammation
  • fibrosis
  • epigenetics
  • non-coding RNAs
  • immunometabolism
  • single-cell transcriptomics
  • angiogenesis
  • ischemic preconditioning
  • nanomedicine
  • molecular cardiology
  • targeted therapy

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

16 pages, 9263 KB  
Article
Immunohistochemical Characterization and CT-Derived Volume of Epicardial Adipose Tissue in Patients with Coronary Artery Disease
by Matija Furtula, Igor Zivkovic, Slobodan Micovic, Zoran Tabakovic, Gorica Vidovic, Zelimir Antonic, Jelica Vukmirovic, David Savic, Milovan Bojic, Branko Beleslin, Milan Dobric and Jelena Rakocevic
Cells 2025, 14(22), 1760; https://doi.org/10.3390/cells14221760 - 11 Nov 2025
Viewed by 436
Abstract
Background: Epicardial adipose tissue (EAT) is a visceral fat depot surrounding the myocardium. It contributes to coronary artery disease (CAD) through local inflammation, while its metabolic activity, including the expression of uncoupling protein-1 (UCP-1) and incretin receptors (GLP-1R, GIPR), may exert protective effects. [...] Read more.
Background: Epicardial adipose tissue (EAT) is a visceral fat depot surrounding the myocardium. It contributes to coronary artery disease (CAD) through local inflammation, while its metabolic activity, including the expression of uncoupling protein-1 (UCP-1) and incretin receptors (GLP-1R, GIPR), may exert protective effects. The relationship between EAT immunohistochemical features and imaging-derived volume remains unclear. Methods: We prospectively studied 50 patients undergoing cardiac surgery: 25 with CAD undergoing coronary artery bypass grafting and 25 without CAD undergoing valve replacement. EAT samples were immunohistochemically stained for CD3, CD68, MPO, UCP-1, GLP-1R, and GIPR. Preoperative CT was used to quantify EAT volume. Results: Patients with CAD more frequently had higher CD3 immunopositivity compared to the control group (84.0 vs. 58.3%, p = 0.047), with no difference in MPO and CD68 immunoexpression. UCP-1 expression was elevated in CAD patients (p = 0.004), whereas GLP-1R and GIPR immunopositivity were similar. EAT volume did not differ between CAD and non-CAD patients (102.87 cm3 vs. 99.38 cm3, p = 0.964) but correlated modestly with BMI (rs = 0.325, p = 0.021). UCP-1 and GLP-1R immunopositivity, as well as larger LVEDD (left ventricular end-diastolic diameter), were positively associated with greater EAT volume. Conclusions: EAT in CAD exhibits increased T-cell infiltration and elevated UCP-1 expression, indicating an inflammatory yet metabolically active profile. Larger EAT volume was associated with UCP-1 and GLP-1R expression, underscoring the immunometabolic role of EAT in CAD. Full article
(This article belongs to the Special Issue Ischemic Heart Disease: From Cellular Level to Clinical Approaches)
Show Figures

Figure 1

Back to TopTop