Molecular Biomarkers in Cardiology 2025

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 1369

Special Issue Editor


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Guest Editor
Cardiology Section, Hospital “F. Perinei” Altamura (BA), 70022 Altamura, Italy
Interests: heart failure; preventive cardiology; vascular biology; endothelial function; cardiovascular pharmacology
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Special Issue Information

Dear Colleagues,

Cardiovascular diseases still represent the leading cause of death worldwide. The need to prevent the acute onset of such diseases and predict their occurrence is the major goal of medicine. By succeeding in preventing the negative consequences of cardiovascular diseases, physicians can prevent both the mortality and morbidity of the patients. Therefore, the improvement in the quality of life and the reduction in the financial burden of health due to the reduced impact of chronic comorbidities related to cardiovascular diseases will also improve the economics of the nations.

The use of biomarkers is the key to conquering the tip of this target mountain.

Indeed, the ideal biomarkers should be sensitive and specific, able to detect the onset of pathologies early and in time to allow physicians to counteract the progression of the disease.

Biomolecular approaches for the early identification of cardiovascular diseases before their onset are an attractive field in cardiology. There is little evidence regarding a perfect biomarker able to identify the unstable atherosclerotic plaque, the occurrence of aortic dissection, or the incipient onset of heart failure.

The aim of this Special Issue is to offer the readers the best overview of the current state of knowledge of biomolecular biomarkers in cardiovascular diseases.

Dr. Pietro Scicchitano
Guest Editor

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Keywords

  • cardiovascular diseases
  • cardiovascular pathology and histology
  • carotid plaques and histology
  • endothelium and endothelial dysfunction
  • veins diseases
  • arrhythmias
  • heart

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Published Papers (1 paper)

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Research

11 pages, 1476 KiB  
Article
The Emerging Role of Colchicine to Inhibit NOD-like Receptor Family, Pyrin Domain Containing 3 Inflammasome and Interleukin-1β Expression in In Vitro Models
by Tri Astiawati, Mohammad Saifur Rohman, Titin Wihastuti, Hidayat Sujuti, Agustina Endharti, Djanggan Sargowo, Delvac Oceandy, Bayu Lestari, Efta Triastuti and Ricardo Adrian Nugraha
Biomolecules 2025, 15(3), 367; https://doi.org/10.3390/biom15030367 - 3 Mar 2025
Viewed by 686
Abstract
While the beneficial effects of colchicine on inflammation and infarcted myocardium have been documented, its impact on cardiac fibroblast activation in the context of myocardial infarction (MI) remains unknown. This study aimed to investigate the effect of colchicine on the regulation of NOD-like [...] Read more.
While the beneficial effects of colchicine on inflammation and infarcted myocardium have been documented, its impact on cardiac fibroblast activation in the context of myocardial infarction (MI) remains unknown. This study aimed to investigate the effect of colchicine on the regulation of NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and Interleukin-1β (IL-1β) expression in fibroblasts. 3T3 fibroblasts were exposed to 600 μM CoCl2 for 24 h to simulate hypoxia, with normoxic cells as controls. Colchicine (1 μM) was administered for 24 h. ASC-NLRP3 colocalization and IL-1β expression were evaluated using immunofluorescence and flow cytometry, respectively. Data were analyzed using t-tests and one-way ANOVA with post hoc tests. Hypoxia treatment significantly induced apoptosis-associated speck-like protein containing a CARD (ASC)-NLRP3 colocalization (p < 0.05). Colchicine treatment of hypoxic 3T3 cells reduced ASC-NLRP3 colocalization, although this reduction was not statistically significant. Additionally, IL-1β expression was significantly inhibited in colchicine-treated hypoxic 3T3 cells compared to those treated with placebo (p < 0.05). The findings of this study indicate that colchicine treatment inhibits the activation of the NLRP3 inflammasome by disrupting the colocalization of ASC and NLRP3, thereby reducing IL-1β expression in CoCl2-treated 3T3 cells. Full article
(This article belongs to the Special Issue Molecular Biomarkers in Cardiology 2025)
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