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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

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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.

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Published Papers (2 papers)

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Research

23 pages, 4169 KiB

Open AccessFeature PaperArticle

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://0-doi-org.brum.beds.ac.uk/10.3390/cells11172629 - 24 Aug 2022

Cited by 3 | Viewed by 1767

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 (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)

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15 pages, 4809 KiB

Open AccessArticle

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://0-doi-org.brum.beds.ac.uk/10.3390/cells11030564 - 06 Feb 2022

Cited by 5 | Viewed by 2313

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 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)

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