Autophagy in COPD

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Autophagy is an important cellular homeostatic process, where cell self-degrades long-lived proteins and damaged sub cellular organelles and proteins with the help of lysosomes in eukaryotic cells. In the past decade, remarkable advances have been made in describing autophagy as clinically relevant target to the treatment of pulmonary diseases. In this review I attempt to provide an overview of autophagy signaling pathway and also summarize the recent studies that suggest direct relevancy and function of autophagy pathway in the Chronic Obstructive Pulmonary Disease (COPD). However, further resolution of autophagic proteins and mechanisms is warranted in specifically designing autophagy-based therapeutic targets in COPD. Introduction Autophagy in COPD Mammalian macroautophagy (hereafter referred as autophagy) is evolutionary conserved degradative pathway that involves the fusion of double membrane autophagosomes and lysosomes for the turnover of free amino acids and fatty acids [1,2]. In addition to this, two other forms of autophagy mechanisms have been described. One type involves the invagination of lysosomal membrane to engulf cytosolic components into intralysosomal vesicles termed as microautophagy [3]. In chaperone-mediated autophagy, proteins with a particular consensus motif (KFERQ) are selectively delivered across the lysosomal membrane for degradation [4]. Autophagy can be upregulated in response to multiple forms of physiological stress including starvation [5], growth factor deprivation [6], reactive oxygen species [7], hypoxia [8], hyperoxia [9,10], endoplasmic reticulum stress [11], DNA damage [12], protein aggregates [13] or pathogens [14]. Therefore, autophagy can be predominantly viewed as a cellular response pathway to a variety of stress stimuli rather than a VRI Cell Signaling, Volume 1, Issue 2, October 2013 nutrient deprivation response pathway. Chronic or acute exposure of the aforementioned stimuli can result in dysregulated or deranged autophagy pathway with the development of several pathological conditions. In this regard stimulant cigarette smoke upon chronic exposure has recently demonstrated an increased expression of autophagy markers in the development of COPD [15,16]. A better understanding for the role of autophagy pathway in COPD will help support in the design of the therapies for the cure of COPD. eISSN 2330-0302 I S S N 2 3 3 0 0 3 0 2 ( O n l i i n e ) ; C O D E N : V R I C A O , V R I C e l l S i g n a l i n g , V e d i c Mini Review DOI: http://dx.doi.org/10.14259/cs.v1i2.68 Article Info: Received: September 25th, 2013; Accepted: October 1st, 2013