Isabel de Lavera , Ana Delgado Pavon , Marina Villanueva Paz , Manuel Oropesa-Avila , Mario de la Mata , Elizabet Alcocer-Gomez , Juan Garrido-Maraver , David Cotan , Monica Alvarez-Cordoba , Jose A Sanchez-Alcazar 1 . Show Affiliations »
Abstract
BACKGROUND: The molecular crosstalk between inflammation and autophagy is an emerging field of research that is essential for the understanding of multicellular organism homeostasis and how these processes influence a variety of pathological conditions. OBJECTIVE: In this review, we briefly describe the relationship between autophagy and inflammasome activation. The central role that mitochondria play in both cellular processes is also discussed. CONCLUSION: Inflammasome and autophagy often modulate each other by common inhibitory mechanisms that are controlled by different input pathways. Thus, inflammasome components coordinate autophagy and autophagy regulates inflammasome activation, making the balance between both processes a fundamental player in cellular homeostasis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
BACKGROUND: The molecular crosstalk between inflammation and autophagy is an emerging field of research that is essential for the understanding of multicellular organism homeostasis and how these processes influence a variety of pathological conditions. OBJECTIVE: In this review, we briefly describe the relationship between autophagy and inflammasome activation. The central role that mitochondria play in both cellular processes is also discussed. CONCLUSION: Inflammasome and autophagy often modulate each other by common inhibitory mechanisms that are controlled by different input pathways. Thus, inflammasome components coordinate autophagy and autophagy regulates inflammasome activation, making the balance between both processes a fundamental player in cellular homeostasis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
Entities: Disease
Keywords:
Autophagy; NLRP3; ROS; cytokines; inflammasome; mitochondria
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Year: 2017
PMID: 27231105 DOI: 10.2174/1389450117666160527143143
Source DB: PubMed Journal: Curr Drug Targets ISSN: 1389-4501 Impact factor: 3.465