Pathophysiology of Signal Transduction in Cardiovascular and Pulmonary Disease II

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

Deadline for manuscript submissions: 31 August 2025 | Viewed by 800

Special Issue Editors


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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

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

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. 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 and reviews in the field of the pathophysiology of signal transduction in cardiovascular and pulmonary disease, written by scientists active in the field.

Dr. Yung-Hsin Yeh
Dr. Ying-Ju Lai
Guest Editors

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Keywords

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

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Published Papers (1 paper)

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Review

17 pages, 623 KiB  
Review
Epithelial Dysfunction in Congenital Diaphragmatic Hernia: Mechanisms, Models and Emerging Therapies
by Ophelia Aubert, Olivia M. Dinwoodie, Richard Wagner and Xingbin Ai
Cells 2025, 14(10), 687; https://doi.org/10.3390/cells14100687 - 9 May 2025
Viewed by 324
Abstract
Congenital diaphragmatic hernia (CDH) is a complex disorder whereby improper formation of the diaphragm allows herniation of the internal organs into the thoracic cavity, resulting in pulmonary hypoplasia among other complications. Although epithelial dysfunction is central to CDH pathology, relatively little attention has [...] Read more.
Congenital diaphragmatic hernia (CDH) is a complex disorder whereby improper formation of the diaphragm allows herniation of the internal organs into the thoracic cavity, resulting in pulmonary hypoplasia among other complications. Although epithelial dysfunction is central to CDH pathology, relatively little attention has been paid to the underlying mechanisms orchestrating epithelial malfunction. Proinflammatory signaling downstream of impaired mechanotransduction due to in utero lung compression has been elucidated to drive epithelial cell phenotypes. This has been illustrated by a reduction in nuclear YAP and the upregulation of NF-kB in CDH models. In this review, we draw from recent findings using emerging technologies to examine epithelial cell mechanisms in CDH and discuss the role of compression as a central and, crucially, sufficient driver of CDH phenotypes. In recognition of the limitations of using genetic knockout models to recapitulate such a heterogenic and etiologically complicated disease, we discuss alternative models such as the established nitrofen rat model, air–liquid interface (ALI) cultures, organoids and ex vivo lung explants. Throughout, we acknowledge the importance of involving mechanical compression in the modeling of CDH in order to faithfully recapitulate the disease. Finally, we explore novel therapeutic strategies from stem cell and regenerative therapies to precision medicine and the importance of defining CDH endotypes in order to guide treatments. Full article
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