Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.9
5.1
Journals
Cells
Special Issues
Pathophysiology of Signal Transduction in Cardiovascular and Pulmonary Disease
share announcement

Pathophysiology of Signal Transduction in Cardiovascular and Pulmonary Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 5833

Special Issue Editors

Dr. Ying-Ju Lai

E-Mail Website
Guest Editor
College of Medicine, Chang Gung University, Taoyuan, Taiwan
Interests: pulmonary hypertension; prostaglandin signaling; endothelial mesenchymal transition; cellular and molecular pathobiology of pulmonary hypertension
Special Issues, Collections and Topics in MDPI journals
Dr. Yung-Hsin Yeh

E-Mail Website
Guest Editor
1. Division of Cardiology, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan
2. College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
Interests: cardiac arrhythmia; heart failure; vascular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The cardiopulmonary system includes the heart, blood vessels and blood, trachea, bronchi, and lungs. The central function of the cardiopulmonary system involves a process that centers upon the connection between the heart and lungs through the pulmonary artery, enabling the efficient movement of blood to and from the lungs, where oxygen and carbon dioxide are exchanged.

Cardiovascular disease and pulmonary disease are complicated. There are a series of molecules and complex intracellular mechanisms in the cells of the heart and blood vessel walls that cause cells to respond inappropriately to external stimulation. Cells involved in the defective regulation respond to changes in their local environment through the activation of molecules. The defects in these mechanisms can lead to cardiovascular disease and pulmonary disease. The study of signal transduction pathways in the cardiopulmonary system is important because it can provide more drug targets and methods for the treatment of cardiovascular disease and pulmonary disease by elucidating the pathophysiology of signal transduction and the coordinated responses of multiple signaling pathways.

This Special Issue focuses on multiple aspects of the signal transduction of cells in the cardiopulmonary system, especially in cardiac arrhythmia and pulmonary hypertension, and will accept original studies, reviews, and technical reports in the field of the pathophysiology of signal transduction in cardiovascular and pulmonary disease, written by scientists active in the field

Dr. Ying-Ju Lai
Dr. Yung-Hsin Yeh
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • cardiac arrhythmia
  • atrium
  • ventricle
  • pulmonary
  • vascular
  • signal transduction

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

23 pages, 4169 KiB  
Article
Integrated Analysis of the microRNA–mRNA Network Predicts Potential Regulators of Atrial Fibrillation in Humans
by Rong Wang, Emre Bektik, Phraew Sakon, Xiaowei Wang, Shanying Huang, Xiangbin Meng, Mo Chen, Wenqiang Han, Jie Chen, Yanhong Wang and Jingquan Zhong
Cells 2022, 11(17), 2629; https://doi.org/10.3390/cells11172629 - 24 Aug 2022
Cited by 3 | Viewed by 2258
Abstract
Atrial fibrillation (AF) is a form of sustained cardiac arrhythmia and microRNAs (miRs) play crucial roles in the pathophysiology of AF. To identify novel miR–mRNA pairs, we performed RNA-seq from atrial biopsies of persistent AF patients and non-AF patients with normal sinus rhythm [...] Read more.
Atrial fibrillation (AF) is a form of sustained cardiac arrhythmia and microRNAs (miRs) play crucial roles in the pathophysiology of AF. To identify novel miR–mRNA pairs, we performed RNA-seq from atrial biopsies of persistent AF patients and non-AF patients with normal sinus rhythm (SR). Differentially expressed miRs (11 down and 9 up) and mRNAs (95 up and 82 down) were identified and hierarchically clustered in a heat map. Subsequently, GO, KEGG, and GSEA analyses were run to identify deregulated pathways. Then, miR targets were predicted in the miRDB database, and a regulatory network of negatively correlated miR–mRNA pairs was constructed using Cytoscape. To select potential candidate genes from GSEA analysis, the top-50 enriched genes in GSEA were overlaid with predicted targets of differentially deregulated miRs. Further, the protein–protein interaction (PPI) network of enriched genes in GSEA was constructed, and subsequently, GO and canonical pathway analyses were run for genes in the PPI network. Our analyses showed that TNF-α, p53, EMT, and SYDECAN1 signaling were among the highly affected pathways in AF samples. SDC-1 (SYNDECAN-1) was the top-enriched gene in p53, EMT, and SYDECAN1 signaling. Consistently, SDC-1 mRNA and protein levels were significantly higher in atrial samples of AF patients. Among negatively correlated miRs, miR-302b-3p was experimentally validated to suppress SDC-1 transcript levels. Overall, our results suggested that the miR-302b-3p/SDC-1 axis may be involved in the pathogenesis of AF. Full article
(This article belongs to the Special Issue Pathophysiology of Signal Transduction in Cardiovascular and Pulmonary Disease)
►▼ Show Figures

Figure 1

15 pages, 4809 KiB  
Article
Dynamic Changes in miR-21 Regulate Right Ventricular Dysfunction in Congenital Heart Disease-Related Pulmonary Arterial Hypertension
by Wei-Ting Chang, Chia-Chun Wu, Yu-Wen Lin, Jhih-Yuan Shih, Zhih-Cherng Chen, Sheng-Nan Wu, Chia-Ching Wu and Chih-Hsin Hsu
Cells 2022, 11(3), 564; https://doi.org/10.3390/cells11030564 - 6 Feb 2022
Cited by 9 | Viewed by 2887
Abstract
Right ventricular (RV) failure is a major cause of mortality in pulmonary arterial hypertension (PAH), but its mechanism remains largely unknown. MicroRNA-21 (miR-21) is involved in flow-mediated stress in the vasculature, but its effects on RV remodeling require investigations. Herein, we aim to [...] Read more.
Right ventricular (RV) failure is a major cause of mortality in pulmonary arterial hypertension (PAH), but its mechanism remains largely unknown. MicroRNA-21 (miR-21) is involved in flow-mediated stress in the vasculature, but its effects on RV remodeling require investigations. Herein, we aim to study the mechanism of miR-21 in the early (compensated) and late (decompensated) phases of PAH-induced RV dysfunction. Using aorto-venous fistula (AVS) surgery, we established a rat model of PAH. To mimic the microenvironment of PAH, we treated cardiomyocytes with flow-mediated shear stress in 6 dyne for 3 and 8 h. To evaluate whether miR-21 could be a biomarker, we prospectively collected the sera of patients with congenital heart disease- (CHD) related PAH. Additionally, clinical, echocardiographic and right heart catheterization information was collected. The primary endpoint was hospitalization for decompensated heart failure (HF). It is of note that, despite an initial increase in miR-21 expression in hypertrophic RV post AVS, miR-21 expression decreased with RV dysfunction thereafter. Likewise, the activation of miR-21 in cardiomyocytes under shear stress at 3 h was downregulated at 6 h. The downregulated miR-21 at the late phase was associated with increased apoptosis in cardiomyocytes while miR-21 mimic rescued it. Among 76 CHD-induced PAH patients, 19 who were hospitalized for heart failure represented with a significantly lower expression of circulating miR-21. Collectively, our study revealed that the upregulation of miR-21 in the early phase (RV hypertrophy) and downregulation in the late phase (RV dysfunction) under PAH triggered a biphasic regulation of cardiac remodeling and cardiomyocyte apoptosis. Full article
(This article belongs to the Special Issue Pathophysiology of Signal Transduction in Cardiovascular and Pulmonary Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop