Topic Editors

Prof. Dr. Pasi Tavi
Cardiovascular Cell Physiology, University of Eastern Finland, Kuopio, Finland
Prof. Dr. Ebru Arioglu-Inan
Department of Pharmacology, Faculty of Pharmacy, Ankara University, Ankara, Turkey

Molecular and Cellular Mechanisms of Heart Disease

Abstract submission deadline
30 September 2026
Manuscript submission deadline
31 December 2026
Viewed by
763

Topic Information

Dear Colleagues,

Heart failure is still a leading cause of mortality worldwide. Cardiomyocytes contribute to heart failure by losing the ability to generate sufficient force to pump blood into circulation. To improve the current treatment options in cardiology, it is important to have a better understanding of the biological behavior of cardiomyocytes. The function of these cells cannot be completely understood independently of the interaction with surrounding cells, i.e., cardiac fibroblasts and vascular cells. Nevertheless, cardiomyocytes are the cells that must generate heart work. They can modify parts of their electromechanical coupling machinery, electrometabolic coupling, or increase in size via hypertrophy. However, hypertrophy can be either adaptive or maladaptive, and the transition from the one into the other type of hypertrophy is not clearly understood. Pathological hypertrophy is often characterised by cardiac fibrosis and contributes to cardiac dysfunction. Cell death, i.e., cardiomyocyte apoptosis, is another common feature of heart disease. Processes dealing with metabolism and mitochondrial function, electromechanical coupling, cell death, and electrophysiological aspects are among the processes that need to be addressed and understood in their molecular fine regulation in order to improve treatment regimes.

This Topic aims to summarize the current understanding of the process of developing heart failure with a focus on the force-generating cell, the cardiomyocyte.

Prof. Dr. Pasi Tavi
Prof. Dr. Ebru Arioglu
Topic Editors

Keywords

  • cardiac metabolism
  • electromechanical coupling
  • regulation of cell death in the heart (apoptosis, autophagy, pyroptosis, ferroptosis, etc.)
  • right heart failure
  • electrophysiological aspects of cardiomyocytes
  • cardiac fibrosis and hypertrophy
  • mitochondrial dysfunction

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Current Issues in Molecular Biology
cimb
2.8 2.9 1999 16.8 Days CHF 2200 Submit
International Journal of Molecular Sciences
ijms
4.9 8.1 2000 18.1 Days CHF 2900 Submit
Journal of Cardiovascular Development and Disease
jcdd
2.4 2.6 2014 22.9 Days CHF 2700 Submit
Organoids
organoids
- - 2022 15.0 days * CHF 1000 Submit
Biomedicines
biomedicines
3.9 5.2 2013 15.3 Days CHF 2600 Submit

* Median value for all MDPI journals in the first half of 2024.


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Published Papers (1 paper)

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12 pages, 694 KiB  
Article
A Multi-Biomarker Approach to Increase the Accuracy of Diagnosis and Management of Coronary Artery Disease
by Lenka Hostačná, Jana Mašlanková, Dominik Pella, Beáta Hubková, Mária Mareková and Daniel Pella
J. Cardiovasc. Dev. Dis. 2024, 11(9), 258; https://doi.org/10.3390/jcdd11090258 - 23 Aug 2024
Viewed by 439
Abstract
Non-invasive possibilities of predicting cardiovascular risk and monitoring the treatment and progression of coronary artery disease (CAD) are important subjects of cardiovascular research. Various inflammatory markers have been identified as potential biomarkers of CAD, including interleukin-6 (IL-6), lipocalin-2 (LCN-2), growth differentiation factor 15 [...] Read more.
Non-invasive possibilities of predicting cardiovascular risk and monitoring the treatment and progression of coronary artery disease (CAD) are important subjects of cardiovascular research. Various inflammatory markers have been identified as potential biomarkers of CAD, including interleukin-6 (IL-6), lipocalin-2 (LCN-2), growth differentiation factor 15 (GDF-15), and T cell immunoglobulin and mucin domain-3 (TIM-3). This research aims to identify their utility in the investigation of CAD severity and progression. The basic anthropometric parameters, as well as the levels of urea, creatinine, CRP, leukocytes, fibrinogen, and biomarkers of inflammation, were measured in 130 patients who underwent coronary angiography. In male patients, divided according to findings on coronary angiography, we observed an increasing expression of GDF-15 with increasing stenosis (with worsening findings). In females, we observed increasing fibrinogen expression with increasing stenosis, i.e., findings on coronary angiography. Correlation analysis did not confirm the relationship between TIM-3, LCN and 2, IL-6 and the severity of findings obtained by coronary angiography; however, the correlation of TIM-3 and LCN-2 expression was positive with the finding, and the correlation of IL-6 with the finding was surprisingly negative. Understanding the role of these inflammatory markers in CAD can be helpful in risk stratification, guiding therapeutic strategies, and monitoring treatment responses in patients with CAD. Full article
(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)
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