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Molecular Insights into Heart Failure: From Bench to Bedside

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: 20 February 2026 | Viewed by 1317

Special Issue Editor


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Guest Editor
Department of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli, IRCCS, 00168 Rome, Italy
Interests: biomarkers; heart failure; ischemic heart disease; preserved ejection fraction; cardiology; fibrosis; inflammation; non-coding RNA
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Special Issue Information

Dear Colleagues,

Significant progress has been made in the understanding of how molecular processes regulate cardiac function and how disruptions in these processes contribute to heart failure. However, there are still some significant gaps in the understanding of disease mechanisms, and further research is needed.

This Special Issue aims to explore the intricate molecular mechanisms that underlie heart failure, bridging the gap between basic research and clinical applications.

Key themes include:

  • Molecular Pathways: This issue aims to examine the complex molecular pathways involved in cardiac hypertrophy, calcium homeostasis, and immune activation during heart failure. We want to highlight the roles of key molecular players, such as signaling molecules, transcriptional regulators, and microRNAs;
  • Translational Research: A strong focus is placed on translating molecular insights into clinical applications, aiming to improve the diagnosis, prognosis, and treatment of heart failure through the development of novel therapeutic targets and strategies based on molecular understanding;
  • Clinical Relevance: This issue addresses the clinical implications of molecular findings, discussing how these insights can be used to personalize medicine and improve patient outcomes.

It also addresses the importance of understanding the molecular differences within different types of heart failure, such as heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF).

In conclusion, this Special Issue aims to provide a comprehensive overview of the latest advancements in molecular research related to heart failure, highlighting the crucial role of these insights in advancing clinical practice.

Dr. Nadia Aspromonte
Guest Editor

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Keywords

  • heart failure
  • cardiac biomarkers
  • medical therapy
  • molecular pathways
  • prognosis
  • target therapy

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Published Papers (1 paper)

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Research

13 pages, 2092 KB  
Article
Evaluation of the Effects of the Sodium–Glucose Cotransporter 2 Inhibitors and Sacubitril/Valsartan Combined Therapy in Patients with HFrEF: An Echocardiographic Study
by Isabella Fumarulo, Annalisa Pasquini, Giulia La Vecchia, Bianca Pellizzeri, Andriy Sten, Barbara Garramone, Marcello Vaccarella, Salvatore Emanuele Ravenna, Antonella Lombardo, Francesco Burzotta, Dario Pitocco and Nadia Aspromonte
Int. J. Mol. Sci. 2025, 26(12), 5651; https://doi.org/10.3390/ijms26125651 - 12 Jun 2025
Cited by 2 | Viewed by 1137
Abstract
Sodium–glucose cotransporter 2 inhibitors (iSGLT2) have become the fourth pillar of the medical treatment for heart failure with reduced ejection fraction (HFrEF). However, the mechanisms of action of iSGLT2 remain poorly understood. The effectiveness of combined ARNI and iSGLT2 therapy in left ventricular [...] Read more.
Sodium–glucose cotransporter 2 inhibitors (iSGLT2) have become the fourth pillar of the medical treatment for heart failure with reduced ejection fraction (HFrEF). However, the mechanisms of action of iSGLT2 remain poorly understood. The effectiveness of combined ARNI and iSGLT2 therapy in left ventricular (LV) remodeling is still under study. We aim to investigate the effects of ARNI + iSGLT2 combination therapy in patients affected by HFrEF in terms of ventricular remodeling using speckle tracking echocardiography (STE). In this observational study, 136 patients with HFrEF taking ARNI were enrolled. All patients were evaluated at baseline (before iSGLT2), at 3 months and at 12 months from the beginning of iSGLT2 therapy. Echocardiographic parameters, including STE analysis and volumetric and LV contractile function indices, were collected at the three timepoints. The objectives were (1) to evaluate the effects of ARNI + iSGLT2 combination therapy on ultrasound (US) measurements; (2) to evaluate the effects on the variation of laboratory data indicative of HF (NT-pro-BNP); and (3) to evaluate the medium-long term impact of the ARNI + iSGLT2 combination therapy in terms of major cardiovascular events (MACVE). After only three months of combined ARNI + iSGLT2 therapy, we reported a significant improvement in ventricular and atrial volumetric indices, systolic function indices and myocardial deformation parameters assessed by STE. We also reported a significant decrease in NTproBNP levels. This trend was confirmed at 12 months follow-up. Furthermore, narrowing down the analysis to patients who were already treated with ARNI when they started taking iSGLT2, we reported similar results in the improvement of US parameters and NTproBNP levels. Our study has shown that the ARNI + iSGLT2 combination therapy leads to a clinical improvement and positive ventricular remodeling. Even the single introduction of additional iSGLT-2 in HFrEF patients on an otherwise optimized therapy resulted in a significant improvement in US and laboratory variables. The results of our study suggest implementing iSGLT-2 therapy as soon as possible, as the structural and functional cardiac improvements achieved by these drugs are achieved in the short term and maintained in the long term. Full article
(This article belongs to the Special Issue Molecular Insights into Heart Failure: From Bench to Bedside)
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