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Molecular Mechanisms and Therapy of Cardiomyopathy

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 2025 | Viewed by 520

Special Issue Editor


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Guest Editor
Biomedical Sciences, Florida State University, Tallahassee, FL 32306, USA
Interests: cardiomyopathies; troponin

Special Issue Information

Dear Colleagues,

Cardiovascular disease is the leading cause of morbidity and mortality globally. Its prevalence necessitates a detailed understanding of the molecular mechanisms underlying cardiomyopathy to develop targeted therapeutic strategies. Several molecular aberrations have been described in cardiomyopathies of all etiologies, including changes in cardiac contractility and morphology, vascular/endothelial dysfunction, mitochondrial and metabolic dysfunction, ischemia/reduced oxygen perfusion, immune cell dysfunction, and epigenetic mechanisms. These molecular mechanisms have yielded several pharmacological treatment strategies for cardiomyopathies of all etiologies. In addition to pharmacological interventions, lifestyle modification (e.g., nutrition/exercise) is now recommended for patients with cardiomyopathy, and several studies have identified molecular changes from such interventions. Thus, investigating the complex molecular aspects of cardiomyopathies is fundamental for identifying the key signaling pathways, genetic and epigenetic factors, and cellular processes that drive disease progression. Improving our knowledge of the mechanistic basis of cardiomyopathies allows for generating novel therapeutic approaches with the goal of improving patient lives.

This Special Issue is supervised by Dr. Maicon Landim-Vieira, who is assisted by the Guest Editor's Assistant Editor Dr. Ann Centner (Florida State University).

Dr. Maicon Landim-Vieira
Guest Editor

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Keywords

  • cardiomyopathy
  • nutrition
  • exercise
  • pharmacology
  • molecular mechanisms

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Published Papers (1 paper)

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Research

13 pages, 8056 KiB  
Article
Transcriptomic Alterations in Spliceosome Components in Advanced Heart Failure: Status of Cardiac-Specific Alternative Splicing Factors
by Isaac Giménez-Escamilla, Lorena Pérez-Carrillo, Irene González-Torrent, Marta Delgado-Arija, Carlota Benedicto, Manuel Portolés, Estefanía Tarazón and Esther Roselló-Lletí
Int. J. Mol. Sci. 2024, 25(17), 9590; https://doi.org/10.3390/ijms25179590 - 4 Sep 2024
Abstract
Heart failure (HF) is associated with global changes in gene expression. Alternative mRNA splicing (AS) is a key regulatory mechanism underlying these changes. However, the whole status of molecules involved in the splicing process in human HF is unknown. Therefore, we analysed the [...] Read more.
Heart failure (HF) is associated with global changes in gene expression. Alternative mRNA splicing (AS) is a key regulatory mechanism underlying these changes. However, the whole status of molecules involved in the splicing process in human HF is unknown. Therefore, we analysed the spliceosome transcriptome in cardiac tissue (n = 36) from control subjects and HF patients (with ischaemic (ICM) and dilated (DCM) cardiomyopathies) using RNA-seq. We found greater deregulation of spliceosome machinery in ICM. Specifically, we showed widespread upregulation of the E and C complex components, highlighting an increase in SNRPD2 (FC = 1.35, p < 0.05) and DHX35 (FC = 1.34, p < 0.001) mRNA levels. In contrast, we observed generalised downregulation of the A complex and cardiac-specific AS factors, such as the multifunctional protein PCBP2 (FC = −1.29, p < 0.001) and the RNA binding proteins QKI (FC = −1.35, p < 0.01). In addition, we found a relationship between SNPRD2 (an E complex component) and the left ventricular mass index in ICM patients (r = 0.779; p < 0.01). On the other hand, we observed the specific underexpression of DDX46 (FC = −1.29), RBM17 (FC = −1.33), SDE2 (FC = −1.35) and RBFOX1 (FC = −1.33), p < 0.05, in DCM patients. Therefore, these aetiology-related alterations may indicate the differential involvement of the splicing process in the development of ICM and DCM. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapy of Cardiomyopathy)
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