Autophagy in Airway Diseases: A New Frontier in Human Asthma?
Abstract
The study of autophagy ('self-eating'), a fundamental cell fate pathway involved in physiological and pathological subcellular processes, opens a newfrontier in the continuous search for novel therapies for human asthma. Asthma is a complex syndrome with different disease phenotypes. Autophagyplays a central role in cell physiology, energy and metabolism, and cell survival.
Autophagy's hallmarks are the formation of double-membrane autophagic autophagosomes and this process is operational in airway epithelial and mesenchymal cells in asthma. Genetic associations betweenautophagy genes and asthma have been observed including single nucleotide polymorphisms in Atg5 which correlate with reduced lung function inasthma. Immune mechanisms important in asthma such as Th2 cells and eosinophils also manifest autophagy. Lastly, we address the role ofautophagy in extracellular matrix deposition and fibrosis in asthmatic airways remodeling, a pathologic process still without effective therapy, and discuss potential pharmacologic inhibitors. We end by offer two opposing but plausible hypotheses as to how autophagy may be directly involved inairway fibrosis.
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