Next Article in Journal
Physical Activity and Sedentary Behaviour Patterns in 326 Persons with COPD before Starting a Pulmonary Rehabilitation: A Cluster Analysis
Next Article in Special Issue
Mucins as a New Frontier in Pulmonary Fibrosis
Previous Article in Journal
Correlation between Sleep Bruxism, Stress, and Depression—A Polysomnographic Study
Previous Article in Special Issue
Pulmonary Fibrosis in Children
Review

Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets

1
Department of Respiratory Diseases, GIGA-I3 Research Group, University and CHU of Liège, 4000 Liège, Belgium
2
Fibropôle Research Group, University and CHU of Liège, 4000 Liège, Belgium
3
Laboratory of Molecular Angiogenesis, GIGA-Cancer Research Group, University of Liège, 4000 Liège, Belgium
4
Department of Gastroenterology, GIGA-I3 Research Group, University and CHU of Liège, 4000 Liège, Belgium
5
Department of Rheumatology, GIGA-I3 Research Group, University and CHU of Liège, 4000 Liège, Belgium
*
Authors to whom correspondence should be addressed.
J. Clin. Med. 2019, 8(9), 1345; https://doi.org/10.3390/jcm8091345
Received: 26 July 2019 / Revised: 26 August 2019 / Accepted: 27 August 2019 / Published: 29 August 2019
(This article belongs to the Special Issue The New Frontier in Pulmonary Fibrosis)
Increasing evidence suggests the potential role of extracellular vesicles (EVs) in many lung diseases. According to their subcellular origin, secretion mechanism, and size, EVs are currently classified into three subpopulations: exosomes, microvesicles, and apoptotic bodies. Exosomes are released in most biofluids, including airway fluids, and play a key role in intercellular communication via the delivery of their cargo (e.g., microRNAs (miRNAs)) to target cell. In a physiological context, lung exosomes present protective effects against stress signals which allow them to participate in the maintenance of lung homeostasis. The presence of air pollution alters the composition of lung exosomes (dysregulation of exosomal miRNAs) and their homeostatic property. Indeed, besides their potential as diagnostic biomarkers for lung diseases, lung exosomes are functional units capable of dysregulating numerous pathophysiological processes (including inflammation or fibrosis), resulting in the promotion of lung disease progression. Here, we review recent studies on the known and potential role of lung exosomes/exosomal miRNAs, in the maintaining of lung homeostasis on one hand, and in promoting lung disease progression on the other. We will also discuss using exosomes as prognostic/diagnostic biomarkers as well as therapeutic tools for lung diseases. View Full-Text
Keywords: exosomes; microRNAs; lung diseases; chronic obstructive pulmonary disease; asthma; acute lung injury/acute respiratory distress syndrome; idiopathic pulmonary fibrosis; diagnostic biomarkers; therapeutics exosomes; microRNAs; lung diseases; chronic obstructive pulmonary disease; asthma; acute lung injury/acute respiratory distress syndrome; idiopathic pulmonary fibrosis; diagnostic biomarkers; therapeutics
Show Figures

Figure 1

MDPI and ACS Style

Guiot, J.; Struman, I.; Louis, E.; Louis, R.; Malaise, M.; Njock, M.-S. Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets. J. Clin. Med. 2019, 8, 1345. https://doi.org/10.3390/jcm8091345

AMA Style

Guiot J, Struman I, Louis E, Louis R, Malaise M, Njock M-S. Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets. Journal of Clinical Medicine. 2019; 8(9):1345. https://doi.org/10.3390/jcm8091345

Chicago/Turabian Style

Guiot, Julien, Ingrid Struman, Edouard Louis, Renaud Louis, Michel Malaise, and Makon-Sébastien Njock. 2019. "Exosomal miRNAs in Lung Diseases: From Biologic Function to Therapeutic Targets" Journal of Clinical Medicine 8, no. 9: 1345. https://doi.org/10.3390/jcm8091345

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop