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Recent Advances in Molecular Pathophysiology of Cardiovascular Diseases 2.0
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Recent Advances in Molecular Pathophysiology of Cardiovascular Diseases 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: closed (5 May 2024) | Viewed by 2215

Special Issue Editor

Prof. Dr. Mirela Cleopatra Tomescu

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Guest Editor
Department of Internal Medicine, Victor Babes University of Medicine and Pharmacy of Timisoara, Timisoara, Romania
Interests: cardiology; coronary artery disease; heart failure; arrhythmias; imaging; echocardiography
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Molecular cardiology is a new and fast-growing area of cardiovascular medicine that aims to apply molecular biology techniques for the mechanistic investigation, diagnosis, prevention, and treatment of cardiovascular disease.

As an emerging discipline, it has changed our conceptual thinking of cardiovascular development, disease etiology and pathophysiology. Although molecular cardiology is still at a very early stage, it constitutes a promising avenue for understanding and controlling cardiovascular disease.

The Special Issue will address the recent advances in the molecular pathophysiology of cardiovascular disease, including gene analysis in injured and hypertrophied hearts; transgenic techniques in cardiac research; gene transfer and gene therapy for cardiovascular disease; and stem cell therapy for cardiovascular disease.

It would be an honor to publish your article in the upcoming Special Issue of our journal. Therefore, we request you consider submitting a manuscript. This Special Issue is supervised by Prof. Dr. Mirela Cleopatra Tomescu and assisted by our Topical Advisory Panel Member, Dr. Sourav Ghorai (University of Illinois at Chicago).

Prof. Dr. Mirela Cleopatra Tomescu
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

  • DNA
  • genes
  • heart diseases
  • hypertrophy
  • molecular biology
  • myocardial infarction

Published Papers (2 papers)

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Research

11 pages, 4201 KiB  
Article
Identification and Functional Verification of CITED2 Gene Promoter Region in Patients with Patent Ductus Arteriosus
by Zhuo Chen, Huan-Xin Chen, Hai-Tao Hou, Xiu-Yun Yin, Qin Yang and Guo-Wei He
Int. J. Mol. Sci. 2023, 24(22), 16204; https://doi.org/10.3390/ijms242216204 - 11 Nov 2023
Viewed by 776
Abstract
Patent ductus arteriosus (PDA) is a common congenital heart disease. CITED2 plays an important role in the development of the heart, and genetic variants in its coding region are significantly associated with cardiac malformations. However, the role of variants in the promoter region [...] Read more.
Patent ductus arteriosus (PDA) is a common congenital heart disease. CITED2 plays an important role in the development of the heart, and genetic variants in its coding region are significantly associated with cardiac malformations. However, the role of variants in the promoter region of CITED2 in the development of PDA remains unclear. We extracted the peripheral blood of 646 subjects (including 353 PDA patients and 293 unrelated healthy controls) for sequencing. We identified 13 promoter variants of the CITED2 gene (including 2 novel heterozygous variants). Of the 13 variants, 10 were found only in PDA patients. In mouse cardiomyocytes (HL-1) and rat cardiac myocytes (RCM), the transcriptional activity of the CITED2 gene promoter was significantly changed by the variants (p < 0.05). The results of the experiments of electrophoretic mobility indicated that these variants may affect the transcription of the CITED2 gene by influencing the binding ability of transcription factors. These results, combined with the JASPAR database analysis, showed that the destruction/production of transcription factor binding sites due to the variants in the promoter region of the CITED2 gene may directly or indirectly affect the binding ability of transcription factors. Our results suggest for the first time that variants at the CITED2 promoter region may cause low expression of CITED2 protein related to the formation of PDA. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Pathophysiology of Cardiovascular Diseases 2.0)
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17 pages, 4371 KiB  
Article
Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis
by María Ortega, Tamara Molina-García, Jose Gavara, Elena de Dios, Nerea Pérez-Solé, Victor Marcos-Garcés, Francisco J. Chorro, Cesar Rios-Navarro, Amparo Ruiz-Sauri and Vicente Bodi
Int. J. Mol. Sci. 2023, 24(21), 15698; https://doi.org/10.3390/ijms242115698 - 28 Oct 2023
Viewed by 867
Abstract
Endothelial cells (ECs) are a key target for cardioprotection due to their role in preserving cardiac microvasculature and homeostasis after myocardial infarction (MI). Our goal is to identify the genes involved in post-MI EC proliferation, EC apoptosis, and angiogenesis regulation via RNA-sequencing transcriptomic [...] Read more.
Endothelial cells (ECs) are a key target for cardioprotection due to their role in preserving cardiac microvasculature and homeostasis after myocardial infarction (MI). Our goal is to identify the genes involved in post-MI EC proliferation, EC apoptosis, and angiogenesis regulation via RNA-sequencing transcriptomic datasets. Using eight studies from the Gene Expression Omnibus, RNA-sequencing data from 92 mice submitted to different times of coronary ischemia or sham were chosen. Functional enrichment analysis was performed based on gene ontology biological processes (BPs). Apoptosis-related BPs are activated up to day 3 after ischemia onset, whereas endothelial proliferation occurs from day 3 onwards, including an overrepresentation of up to 37 genes. Endothelial apoptosis post-MI is triggered via both the extrinsic and intrinsic signaling pathways, as reflected by the overrepresentation of 13 and 2 specific genes, respectively. BPs implicated in new vessel formation are upregulated soon after ischemia onset, whilst the mechanisms aiming at angiogenesis repression can be detected at day 3. Overall, 51 pro-angiogenic and 29 anti-angiogenic factors displayed altered transcriptomic expression post-MI. This is the first study using RNA sequencing datasets to evaluate the genes participating in post-MI endothelium physiology and angiogenesis regulation. These novel data could lay the groundwork to advance understanding of the implication of ECs after MI. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Pathophysiology of Cardiovascular Diseases 2.0)
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