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Mol. Cells 2013; 36(5): 393-399

Published online November 30, 2013

https://doi.org/10.1007/s10059-013-0298-0

© The Korean Society for Molecular and Cellular Biology

Crosstalk between Autophagy and Inflammasomes

Jae-Min Yuk, and Eun-Kyeong Jo

1Department of Microbiology, 2Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, Korea

Received: October 8, 2013; Accepted: October 11, 2013

Abstract

A variety of cellular stresses activate the autophagy pathway, which is fundamentally important in protection against injurious stimuli. Defects in the autophagy process are associated with a variety of human diseases, including inflammatory and metabolic diseases. The inflammasomes are emerging as key signaling platforms directing the maturation and secretion of interleukin-1 family cytokines in response to pathogenic and sterile stimuli. Recent studies have identified the critical role of inflammasome activation in host defense and inflammation. Delineation of the relationship between autophagy and inflammasome activation is now being greatly facilitated by the use of mice models of autophagy gene deficiency and clinical studies. We surveyed the recent research regarding the contribution of autophagy to the control of inflammation, in particular the association between autophagy and inflammasomes. Understanding the mechanisms by which autophagy balances inflammation might facilitate the development of autophagy-based therapeutic modalities for infectious and inflammatory diseases.

Keywords autophagy, host defense, inflammasome, inflammation, NLRP3

Article

Minireview

Mol. Cells 2013; 36(5): 393-399

Published online November 30, 2013 https://doi.org/10.1007/s10059-013-0298-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Crosstalk between Autophagy and Inflammasomes

Jae-Min Yuk, and Eun-Kyeong Jo

1Department of Microbiology, 2Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, Korea

Received: October 8, 2013; Accepted: October 11, 2013

Abstract

A variety of cellular stresses activate the autophagy pathway, which is fundamentally important in protection against injurious stimuli. Defects in the autophagy process are associated with a variety of human diseases, including inflammatory and metabolic diseases. The inflammasomes are emerging as key signaling platforms directing the maturation and secretion of interleukin-1 family cytokines in response to pathogenic and sterile stimuli. Recent studies have identified the critical role of inflammasome activation in host defense and inflammation. Delineation of the relationship between autophagy and inflammasome activation is now being greatly facilitated by the use of mice models of autophagy gene deficiency and clinical studies. We surveyed the recent research regarding the contribution of autophagy to the control of inflammation, in particular the association between autophagy and inflammasomes. Understanding the mechanisms by which autophagy balances inflammation might facilitate the development of autophagy-based therapeutic modalities for infectious and inflammatory diseases.

Keywords: autophagy, host defense, inflammasome, inflammation, NLRP3

Mol. Cells
Sep 30, 2022 Vol.45 No.9, pp. 603~672
COVER PICTURE
The Target of Rapamycin Complex (TORC) is a central regulatory hub in eukaryotes, which is well conserved in diverse plant species, including tomato (Solanum lycopersicum). Inhibition of TORC genes (SlTOR, SlLST8, and SlRAPTOR) by VIGS (virus-induced gene silencing) results in early fruit ripening in tomato. The red/ orange tomatoes are early-ripened TORC-silenced fruits, while the green tomato is a control fruit. Top, left, control fruit (TRV2-myc); top, right, TRV2-SlLST8; bottom, left, TRV2-SlTOR; bottom, right, TRV2-SlRAPTOR(Choi et al., pp. 660-672).

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