Abstract
Mechanical stress plays a critical role among development, functional maturation, and pathogenesis of pulmonary tissues, especially for the alveolar epithelial cells and vascular endothelial cells located in the microenvironment established with vascular network and bronchial-alveolar network. Alveolar epithelial cells are mainly loaded by cyclic strain and air pressure tension. While vascular endothelial cells are exposed to shear stress and cyclic strain. Currently, the emerging evidences demonstrated that non-physiological mechanical forces would lead to several pulmonary diseases, including pulmonary hypertension, fibrosis, and ventilation induced lung injury. Furthermore, a series of intracellular signaling had been identified to be involved in mechanotransduction and participated in regulating the physiological homeostasis and pathophysiological process. Besides, the communications between alveolar epithelium and vascular endothelium under non-physiological stress contribute to the remodeling of the pulmonary micro-environment in collaboration, including hypoxia induced injuries, endothelial permeability impairment, extracellular matrix stiffness elevation, metabolic alternation, and inflammation activation. In this review, we aim to summarize the current understandings of mechanotransduction on the relation between mechanical forces acting on the lung and biological response in mechanical overloading related diseases. We also would like to emphasize the interplays between alveolar epithelium and vascular endothelium, providing new insights into pulmonary diseases pathogenesis, and potential targets for therapy.
Highlights
As an area of gas exchange, the lung has extensive vascular and bronchial–alveolar networks and displays tension properties after birth
Zeinali et al (2021) developed an in vitro three-dimensional (3D) microvessel model to investigate the effects of the 3D mechanical cyclic stretch of different magnitudes and vascular endothelial growth factor (VEGF) stimulation on a 3D perfusing vasculature; the results shows that physiological cyclic stretch restored the vascular barrier tightness and significantly decreases vascular permeability (Zeinali et al, 2021)
Lung serves as the places for gas exchange, alveoli and blood vessels are essential for such biological process
Summary
As an area of gas exchange, the lung has extensive vascular and bronchial–alveolar networks and displays tension properties after birth. The pulmonary pressure gradient of the lung fluid increases the elasticity of the fetal lung tissues and stimulates the lung epithelial cells to actively secrete chloride ions. These chloride ions are transported into the stroma and the lung cavity by blood. Endothelial cells, fibroblasts, and smooth muscle cells are continuously stimulated in the pulmonary arteries by mechanical forces such as shear stress and pulsatile blood pressure. Cyclic stretching stimulates lung development as a result of breathing movements and shear stress induced by blood flow, which act on the PAECs and the alveolar epithelium
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