Participation of Mesenchymal Stem Cells in Acute Lung Injury/Acute Respiratory Distress Syndrome: Paracrine Effects and Transplantation

摘要

Mesenchymal stem cells are a promising source of regenerative cells, and have been used for clinical cell therapy in recent years. Their widespread application originates from established potency in a broad range of experimental animal models and believable safety profile in humans. Acute lung injury/acute respiratory distress syndrome are common and potentially lethal diseases characterized by acute respiratory failure due to noncardiogenic pulmonary edema, excessive pulmonary inflammation, and alveolar-capillary barrier disruption. Despite tremendous research concerning the pathophysiology of acute lung injury, its death rate remains high and seldom efficacious pharmacotherapy exists. Mesenchymal stem cells participate in related mechanisms through paracrine effects by inducing other cells or regulating certain pro-inflammatory and anti-inflammatory factors, and have the trend for re-epithelization and repairment in lung injury by transplanting ability. The paracrine effects of mesenchymal stem cells in these pathways are the current research hotspot by releasing soluble bioactive factors to interact with damaged tissues. Mesenchymal stem cells secrete a broad range of cytokines, growth factors, chemokines, and miRNAs through microvesicles or exosomes to protect endogenous cells, attenuate the inflammatory response and inhibit apoptosis, which may be the therapeutic basis of their application in acute lung injury. Therefore, it is vital to study the effects of mesenchymal stem cells and revealing their mechanisms at the cellular and molecular levels. Their transplantation and differentiation capabilities, as well as the paracrine effects provide pre-clinical basis to prevent and treat acute lung injury/acute respiratory distress syndrome. Several clinical trials have been administrated and mesenchymal stem cells have promising prospects as therapeutic drugs for lung diseases.