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Genetic Basis and Molecular Mechanisms of Heart Failure
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Genetic Basis and Molecular Mechanisms of 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 October 2024 | Viewed by 1534

Special Issue Editors

Prof. Dr. Massimo Volpe

E-Mail Website
Guest Editor
Cardiology Unit, Department of Clinical and Molecular Medicine, Sapienza University of Rome, Sant’Andrea Hospital, Via di Grottarossa 1035, 00189 Rome, Italy
Interests: hypertension; heart failure; neurohormonal systems; cardiovascular prevention
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanna Gallo

E-Mail Website
Guest Editor
Department of Clinical and Molecular Medicine, Sant’Andrea Hospital, Sapienza University of Rome, Via di Grottarossa 1035, 00189 Rome, Italy
Interests: hypertension; heart failure; neurohormonal systems; cardiovascular prevention

Special Issue Information

Dear Colleagues,

A wealth of evidence has demonstrated the relevance of gene mutations and molecular pathways in the development of heart failure, although their contribution is heterogenous and complex. Indeed, the role of genetics ranges from monogenic syndromes caused by single underlying pathogenetic mutations, to complex traits determined by the combination of multiple genetic or epigenetic individually low-penetrance loci with environmental triggers. The risk and course of heart failure depends on underlying genomic variants and mutations. As a consequence, genetic testing is starting to be applied in clinical routine diagnostics to evaluate risk, to predict prognosis and to guide treatment.

This Special Issue of the International Journal of Molecular Sciences focuses on the genetic basis and molecular mechanism of heart failure, and welcomes both original research articles and review papers.

Prof. Dr. Massimo Volpe
Dr. Giovanna Gallo
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • heart failure
  • cardiomyopathies
  • genetics
  • molecular pathways
  • epigenetics
  • gene mutations

Published Papers (1 paper)

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Review

17 pages, 1480 KiB  
Review
Potential Mechanisms of the Protective Effects of the Cardiometabolic Drugs Type-2 Sodium–Glucose Transporter Inhibitors and Glucagon-like Peptide-1 Receptor Agonists in Heart Failure
by Giovanna Gallo and Massimo Volpe
Int. J. Mol. Sci. 2024, 25(5), 2484; https://doi.org/10.3390/ijms25052484 - 20 Feb 2024
Viewed by 1274
Abstract
Different multifactorial pathophysiological processes are involved in the development of heart failure (HF), including neurohormonal dysfunction, the hypertrophy of cardiomyocytes, interstitial fibrosis, microvascular endothelial inflammation, pro-thrombotic states, oxidative stress, decreased nitric oxide (NO) bioavailability, energetic dysfunction, epicardial coronary artery lesions, coronary microvascular rarefaction [...] Read more.
Different multifactorial pathophysiological processes are involved in the development of heart failure (HF), including neurohormonal dysfunction, the hypertrophy of cardiomyocytes, interstitial fibrosis, microvascular endothelial inflammation, pro-thrombotic states, oxidative stress, decreased nitric oxide (NO) bioavailability, energetic dysfunction, epicardial coronary artery lesions, coronary microvascular rarefaction and, finally, cardiac remodeling. While different pharmacological strategies have shown significant cardiovascular benefits in HF with reduced ejection fraction (HFrEF), there is a residual unmet need to fill the gap in terms of knowledge of mechanisms and efficacy in the outcomes of neurohormonal agents in HF with preserved ejection fraction (HFpEF). Recently, type-2 sodium–glucose transporter inhibitors (SGLT2i) have been shown to contribute to a significant reduction in the composite outcome of HF hospitalizations and cardiovascular mortality across the entire spectrum of ejection fraction. Moreover, glucagon-like peptide-1 receptor agonists (GLP1-RA) have demonstrated significant benefits in patients with high cardiovascular risk, excess body weight or obesity and HF, in particular HFpEF. In this review, we will discuss the biological pathways potentially involved in the action of SGLT2i and GLP1-RA, which may explain their effective roles in the treatment of HF, as well as the potential implications of the use of these agents, also in combination therapies with neurohormonal agents, in the clinical practice. Full article
(This article belongs to the Special Issue Genetic Basis and Molecular Mechanisms of Heart Failure)
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