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2015 ; 4
(ä): 215-25
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Autophagy in lung disease pathogenesis and therapeutics
#MMPMID25617802
Ryter SW
; Choi AM
Redox Biol
2015[]; 4
(ä): 215-25
PMID25617802
show ga
Autophagy, a cellular pathway for the degradation of damaged organelles and
proteins, has gained increasing importance in human pulmonary diseases, both as a
modulator of pathogenesis and as a potential therapeutic target. In this pathway,
cytosolic cargos are sequestered into autophagosomes, which are delivered to the
lysosomes where they are enzymatically degraded and then recycled as metabolic
precursors. Autophagy exerts an important effector function in the regulation of
inflammation, and immune system functions. Selective pathways for autophagic
degradation of cargoes may have variable significance in disease pathogenesis.
Among these, the autophagic clearance of bacteria (xenophagy) may represent a
crucial host defense mechanism in the pathogenesis of sepsis and inflammatory
diseases. Our recent studies indicate that the autophagic clearance of
mitochondria, a potentially protective program, may aggravate the pathogenesis of
chronic obstructive pulmonary disease by activating cell death programs. We
report similar findings with respect to the autophagic clearance of cilia
components, which can contribute to airways dysfunction in chronic lung disease.
In certain diseases such as pulmonary hypertension, autophagy may confer
protection by modulating proliferation and cell death. In other disorders, such
as idiopathic pulmonary fibrosis and cystic fibrosis, impaired autophagy may
contribute to pathogenesis. In lung cancer, autophagy has multiple consequences
by limiting carcinogenesis, modulating therapeutic effectiveness, and promoting
tumor cell survival. In this review we highlight the multiple functions of
autophagy and its selective autophagy subtypes that may be of significance to the
pathogenesis of human disease, with an emphasis on lung disease and therapeutics.
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