Crosstalk Between ER Stress, Autophagy and Inflammation

The endoplasmic reticulum (ER) is not only responsible for protein synthesis and folding but also plays a critical role in sensing cellular stress and maintaining cellular homeostasis. Upon sensing the accumulation of unfolded proteins due to perturbation in protein synthesis or folding, specific in...

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Autores principales:	Sandhya Chipurupalli, Unni Samavedam, Nirmal Robinson
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	autophagy unfolded protein response ER-stress cytokines inflammation Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/a5be108ecd404fb39c1d4321d04d161e
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id	oai:doaj.org-article:a5be108ecd404fb39c1d4321d04d161e
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spelling	oai:doaj.org-article:a5be108ecd404fb39c1d4321d04d161e2021-11-05T09:05:04ZCrosstalk Between ER Stress, Autophagy and Inflammation2296-858X10.3389/fmed.2021.758311https://doaj.org/article/a5be108ecd404fb39c1d4321d04d161e2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fmed.2021.758311/fullhttps://doaj.org/toc/2296-858XThe endoplasmic reticulum (ER) is not only responsible for protein synthesis and folding but also plays a critical role in sensing cellular stress and maintaining cellular homeostasis. Upon sensing the accumulation of unfolded proteins due to perturbation in protein synthesis or folding, specific intracellular signaling pathways are activated, which are collectively termed as unfolded protein response (UPR). UPR expands the capacity of the protein folding machinery, decreases protein synthesis and enhances ER-associated protein degradation (ERAD) which degrades misfolded proteins through the proteasomes. More recent evidences suggest that UPR also amplifies cytokines-mediated inflammatory responses leading to pathogenesis of inflammatory diseases. UPR signaling also activates autophagy; a lysosome-dependent degradative pathwaythat has an extended capacity to degrade misfolded proteins and damaged ER. Thus, activation of autophagy limits inflammatory response and provides cyto-protection by attenuating ER-stress. Here we review the mechanisms that couple UPR, autophagy and cytokine-induced inflammation that can facilitate the development of novel therapeutic strategies to mitigate cellular stress and inflammation associated with various pathologies.Sandhya ChipurupalliUnni SamavedamNirmal RobinsonFrontiers Media S.A.articleautophagyunfolded protein responseER-stresscytokinesinflammationMedicine (General)R5-920ENFrontiers in Medicine, Vol 8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	autophagy unfolded protein response ER-stress cytokines inflammation Medicine (General) R5-920
spellingShingle	autophagy unfolded protein response ER-stress cytokines inflammation Medicine (General) R5-920 Sandhya Chipurupalli Unni Samavedam Nirmal Robinson Crosstalk Between ER Stress, Autophagy and Inflammation
description	The endoplasmic reticulum (ER) is not only responsible for protein synthesis and folding but also plays a critical role in sensing cellular stress and maintaining cellular homeostasis. Upon sensing the accumulation of unfolded proteins due to perturbation in protein synthesis or folding, specific intracellular signaling pathways are activated, which are collectively termed as unfolded protein response (UPR). UPR expands the capacity of the protein folding machinery, decreases protein synthesis and enhances ER-associated protein degradation (ERAD) which degrades misfolded proteins through the proteasomes. More recent evidences suggest that UPR also amplifies cytokines-mediated inflammatory responses leading to pathogenesis of inflammatory diseases. UPR signaling also activates autophagy; a lysosome-dependent degradative pathwaythat has an extended capacity to degrade misfolded proteins and damaged ER. Thus, activation of autophagy limits inflammatory response and provides cyto-protection by attenuating ER-stress. Here we review the mechanisms that couple UPR, autophagy and cytokine-induced inflammation that can facilitate the development of novel therapeutic strategies to mitigate cellular stress and inflammation associated with various pathologies.
format	article
author	Sandhya Chipurupalli Unni Samavedam Nirmal Robinson
author_facet	Sandhya Chipurupalli Unni Samavedam Nirmal Robinson
author_sort	Sandhya Chipurupalli
title	Crosstalk Between ER Stress, Autophagy and Inflammation
title_short	Crosstalk Between ER Stress, Autophagy and Inflammation
title_full	Crosstalk Between ER Stress, Autophagy and Inflammation
title_fullStr	Crosstalk Between ER Stress, Autophagy and Inflammation
title_full_unstemmed	Crosstalk Between ER Stress, Autophagy and Inflammation
title_sort	crosstalk between er stress, autophagy and inflammation
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/a5be108ecd404fb39c1d4321d04d161e
work_keys_str_mv	AT sandhyachipurupalli crosstalkbetweenerstressautophagyandinflammation AT unnisamavedam crosstalkbetweenerstressautophagyandinflammation AT nirmalrobinson crosstalkbetweenerstressautophagyandinflammation
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Crosstalk Between ER Stress, Autophagy and Inflammation

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