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Current Research for Heart Disease Biology and Therapeutics 2.0
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Current Research for Heart Disease Biology and Therapeutics 2.0

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: 29 September 2024 | Viewed by 1728

Special Issue Editor

Dr. Claudia Kusmic

E-Mail Website
Guest Editor
Insitute of Clinical Physiology, National Research Council (IFC-CNR), 56124 Pisa, Italy
Interests: preclinical models; in vivo models of cardiac hypertrophy and cardiotoxicity; cardiovascular disease; obesity; mitochondrial damage; cardio-oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

“Heart disease” refers to several types of heart conditions. For example, pathological cardiac hypertrophy is a key risk factor for heart failure. Increased interstitial fibrosis, cardiac dysfunction and cell death are essential features of pathological cardiac hypertrophy. Numerous mediators have been found to be involved in the pathogenesis of maladaptive heart growth, and they can affect gene transcription, calcium handling, protein synthesis, metabolism, mitochondrial function, autophagy, oxidative stress and inflammation. Many of the molecular mechanisms and dysregulated signaling pathways implicated in promoting malignant remodeling have been unrevealed. Focusing on these key regulation points seems to be an important target for defining innovative strategies for the management of heart disease.

This Special Issue aims to take stock of advances in the development and validation of therapeutic strategies against heart disease. Research papers and up-to-date review articles are welcome on various topics including, but not limited to, conventional drug strategies or novel therapeutic approaches (e.g., RNA-based therapies, dietary supplementation, drug delivery systems) targeting molecular pathways involved in the transition to heart disease.

Dr. Claudia Kusmic
Guest Editor

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

  • myocardial hypertrophy
  • cardiac remodeling
  • heart failure
  • drug therapy
  • molecular therapeutic targets
  • myocardial gene therapy
  • heart disease

Published Papers (3 papers)

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Review

19 pages, 867 KiB  
Review
Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis
by Laura Pilar Aguado-Alvaro, Nerea Garitano and Beatriz Pelacho
Int. J. Mol. Sci. 2024, 25(11), 6004; https://doi.org/10.3390/ijms25116004 - 30 May 2024
Viewed by 62
Abstract
Cardiac fibrosis, a process characterized by excessive extracellular matrix (ECM) deposition, is a common pathological consequence of many cardiovascular diseases (CVDs) normally resulting in organ failure and death. Cardiac fibroblasts (CFs) play an essential role in deleterious cardiac remodeling and dysfunction. In response [...] Read more.
Cardiac fibrosis, a process characterized by excessive extracellular matrix (ECM) deposition, is a common pathological consequence of many cardiovascular diseases (CVDs) normally resulting in organ failure and death. Cardiac fibroblasts (CFs) play an essential role in deleterious cardiac remodeling and dysfunction. In response to injury, quiescent CFs become activated and adopt a collagen-secreting phenotype highly contributing to cardiac fibrosis. In recent years, studies have been focused on the exploration of molecular and cellular mechanisms implicated in the activation process of CFs, which allow the development of novel therapeutic approaches for the treatment of cardiac fibrosis. Transcriptomic analyses using single-cell RNA sequencing (RNA-seq) have helped to elucidate the high cellular diversity and complex intercellular communication networks that CFs establish in the mammalian heart. Furthermore, a significant body of work supports the critical role of epigenetic regulation on the expression of genes involved in the pathogenesis of cardiac fibrosis. The study of epigenetic mechanisms, including DNA methylation, histone modification, and chromatin remodeling, has provided more insights into CF activation and fibrotic processes. Targeting epigenetic regulators, especially DNA methyltransferases (DNMT), histone acetylases (HAT), or histone deacetylases (HDAC), has emerged as a promising approach for the development of novel anti-fibrotic therapies. This review focuses on recent transcriptomic advances regarding CF diversity and molecular and epigenetic mechanisms that modulate the activation process of CFs and their possible clinical applications for the treatment of cardiac fibrosis. Full article
(This article belongs to the Special Issue Current Research for Heart Disease Biology and Therapeutics 2.0)
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32 pages, 1356 KiB  
Review
Is Cardiac Transplantation Still a Contraindication in Patients with Muscular Dystrophy-Related End-Stage Dilated Cardiomyopathy? A Systematic Review
by Luisa Politano
Int. J. Mol. Sci. 2024, 25(10), 5289; https://doi.org/10.3390/ijms25105289 - 13 May 2024
Viewed by 549
Abstract
Inherited muscular diseases (MDs) are genetic degenerative disorders typically caused by mutations in a single gene that affect striated muscle and result in progressive weakness and wasting in affected individuals. Cardiac muscle can also be involved with some variability that depends on the [...] Read more.
Inherited muscular diseases (MDs) are genetic degenerative disorders typically caused by mutations in a single gene that affect striated muscle and result in progressive weakness and wasting in affected individuals. Cardiac muscle can also be involved with some variability that depends on the genetic basis of the MD (Muscular Dystrophy) phenotype. Heart involvement can manifest with two main clinical pictures: left ventricular systolic dysfunction with evolution towards dilated cardiomyopathy and refractory heart failure, or the presence of conduction system defects and serious life-threatening ventricular arrhythmias. The two pictures can coexist. In these cases, heart transplantation (HTx) is considered the most appropriate option in patients who are not responders to the optimized standard therapeutic protocols. However, cardiac transplant is still considered a relative contraindication in patients with inherited muscle disorders and end-stage cardiomyopathies. High operative risk related to muscle impairment and potential graft involvement secondary to the underlying myopathy have been the two main reasons implicated in the generalized reluctance to consider cardiac transplant as a viable option. We report an overview of cardiac involvement in MDs and its possible association with the underlying molecular defect, as well as a systematic review of HTx outcomes in patients with MD-related end-stage dilated cardiomyopathy, published so far in the literature. Full article
(This article belongs to the Special Issue Current Research for Heart Disease Biology and Therapeutics 2.0)
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22 pages, 1370 KiB  
Review
Mechanisms of Pulmonary Vasculopathy in Acute and Long-Term COVID-19: A Review
by Marianne Riou, Florence Coste, Alain Meyer, Irina Enache, Samy Talha, Anne Charloux, Cyril Reboul and Bernard Geny
Int. J. Mol. Sci. 2024, 25(9), 4941; https://doi.org/10.3390/ijms25094941 - 30 Apr 2024
Viewed by 1025
Abstract
Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 [...] Read more.
Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID. Full article
(This article belongs to the Special Issue Current Research for Heart Disease Biology and Therapeutics 2.0)
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