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Molecular Research into Chronic Heart Failure

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: 31 January 2026 | Viewed by 1861

Special Issue Editor


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Guest Editor
Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy
Interests: chronic heart failure

Special Issue Information

Dear Colleagues,  

Heart failure represents the epidemic of the third millennium in terms of prevalence, costs, and mortality. Despite prevention, efficient screening, and early-treatment programs, heart failure is still a major problem for both physicians and healthcare systems. At the molecular level, heart failure involves intricate mechanisms of cardiac remodeling, including cardiomyocyte hypertrophy, apoptosis, and fibrosis. This Special Issue, titled “Molecular Research into Chronic Heart Failure”, aims to stimulate comprehensive research to understand the molecular mechanism involved in cardiac remodeling.  This Special Issue will accept articles on the pathophysiology of heart failure, its etiology, and the molecular mechanisms underlying it. This Special Issue aims to focus on basic science, translational research, and clinical evidence in order to gain a more comprehensive understanding of the pathophysiology of heart failure, considering all aspects of this complex puzzle. We look forward to receiving your contributions. 

Dr. Velia Cassano
Guest Editor

Manuscript Submission Information

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Keywords

  • heart failure
  • oxidative stress
  • cardiac remodeling
  • cardiomyopathy
  • proteomic
  • molecular science

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Published Papers (2 papers)

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Research

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18 pages, 8731 KB  
Article
Identification of Connexin 26 on Extracellular Vesicles from Human Cardiomyocytes and Plasma: Novel Insights into miRNA Loading and Oxidative Injury
by Letizia Mattii, Alessandra Falleni, Enza Polizzi, Antonella Cecchettini, Antonietta R. Sabbatini, Manuela Cabiati, Silvia Del Ry, Valentina Casieri, Vincenzo Lionetti, Federico Vozzi, Stefania Moscato and Rosalinda Madonna
Int. J. Mol. Sci. 2025, 26(20), 10128; https://doi.org/10.3390/ijms262010128 - 17 Oct 2025
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Abstract
Connexin 26 (Cx26), a gap junction protein, is poorly understood in the context of cardiac milieu, including extracellular vesicles (EVs). Here, we report for the first time the presence of Cx26 on EVs obtained from human induced pluripotent stem cell-derived cardiomyocytes and human [...] Read more.
Connexin 26 (Cx26), a gap junction protein, is poorly understood in the context of cardiac milieu, including extracellular vesicles (EVs). Here, we report for the first time the presence of Cx26 on EVs obtained from human induced pluripotent stem cell-derived cardiomyocytes and human plasma. Using an in vitro model of oxidative stress and apoptosis in dH9c2 cardiomyocytes, we observed a significant decrease in Cx26 levels in EVs released by injured cells, accompanied by changes in EV concentration, particularly in exosomes. Our findings revealed that Cx26 modulates the selective loading of specific microRNAs, namely miR-1 and miR-30a, into EVs, suggesting a novel non-canonical, gap junction-independent role of Cx26 in EV-mediated cardiac signaling. Analysis of plasma EVs from healthy donors confirmed the presence of Cx26-positive EVs of cardiomyocyte origin, indicated by co-staining with cardiac troponin T. These findings suggest that further studies on the measurement of Cx26 on circulating EVs from patients with ischemic heart disease and heart failure are warranted to clarify its potential as a biomarker for cardiomyocyte injury in cardiomyopathies with oxidative stress and apoptosis. Full article
(This article belongs to the Special Issue Molecular Research into Chronic Heart Failure)
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Review

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15 pages, 929 KB  
Review
Impact of Anabolic–Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications
by Antoni Borowiec, Iga Waluszewska, Michał Jurkiewicz and Wioletta Szczurek-Wasilewicz
Int. J. Mol. Sci. 2025, 26(22), 11037; https://doi.org/10.3390/ijms262211037 - 14 Nov 2025
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Abstract
Anabolic–androgenic steroids (AAS) are synthetic derivatives of testosterone that are used therapeutically but are frequently abused by athletes and individuals seeking to increase muscle mass. Their anabolic (promoting muscle growth) and androgenic (inducing masculine characteristics) effects result from androgen receptor activation in target [...] Read more.
Anabolic–androgenic steroids (AAS) are synthetic derivatives of testosterone that are used therapeutically but are frequently abused by athletes and individuals seeking to increase muscle mass. Their anabolic (promoting muscle growth) and androgenic (inducing masculine characteristics) effects result from androgen receptor activation in target tissues. However, chronic supraphysiological AAS exposure is associated with serious cardiovascular consequences, ranging from hypertension and lipid disorders to cardiomyopathy, atherosclerosis, and sudden cardiac death. This review provides an updated and integrative perspective on both the molecular and clinical aspects of AAS-induced cardiovascular toxicity, highlighting recent advances in understanding endothelial injury, oxidative stress, fibrosis, and arrhythmogenesis. Importantly, it emphasizes the emerging recognition of AAS abuse as a modifiable cardiovascular risk factor and discusses potential preventive and therapeutic strategies, including early cardiovascular screening and risk stratification. Understanding these mechanisms is essential for recognizing the clinical manifestations of AAS misuse and for improving cardiovascular risk assessment in affected individuals. These insights underscore the clinical significance of AAS abuse as a cardiovascular risk factor and the need for vigilant cardiac monitoring and early intervention in this population. Full article
(This article belongs to the Special Issue Molecular Research into Chronic Heart Failure)
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