Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction

Protein transcription, translation, and folding occur continuously in every living cell and are essential for physiological functions. About one-third of all proteins of the cellular proteome interacts with the endoplasmic reticulum (ER). The ER is a large, dynamic cellular organelle that orchestrat...

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Autores principales:	Vitalii Kryvenko, István Vadász
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	hypercapnia carbon dioxide endoplasmic reticulum protein folding unfolded protein response Physiology QP1-981
Acceso en línea:	https://doaj.org/article/30e9f3fa8d0e470690a5bcd0835f3293
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spelling	oai:doaj.org-article:30e9f3fa8d0e470690a5bcd0835f32932021-11-19T07:53:41ZMechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction1664-042X10.3389/fphys.2021.735580https://doaj.org/article/30e9f3fa8d0e470690a5bcd0835f32932021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.735580/fullhttps://doaj.org/toc/1664-042XProtein transcription, translation, and folding occur continuously in every living cell and are essential for physiological functions. About one-third of all proteins of the cellular proteome interacts with the endoplasmic reticulum (ER). The ER is a large, dynamic cellular organelle that orchestrates synthesis, folding, and structural maturation of proteins, regulation of lipid metabolism and additionally functions as a calcium store. Recent evidence suggests that both acute and chronic hypercapnia (elevated levels of CO2) impair ER function by different mechanisms, leading to adaptive and maladaptive regulation of protein folding and maturation. In order to cope with ER stress, cells activate unfolded protein response (UPR) pathways. Initially, during the adaptive phase of ER stress, the UPR mainly functions to restore ER protein-folding homeostasis by decreasing protein synthesis and translation and by activation of ER-associated degradation (ERAD) and autophagy. However, if the initial UPR attempts for alleviating ER stress fail, a maladaptive response is triggered. In this review, we discuss the distinct mechanisms by which elevated CO2 levels affect these molecular pathways in the setting of acute and chronic pulmonary diseases associated with hypercapnia.Vitalii KryvenkoVitalii KryvenkoIstván VadászIstván VadászIstván VadászFrontiers Media S.A.articlehypercapniacarbon dioxideendoplasmic reticulumprotein foldingunfolded protein responsePhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	hypercapnia carbon dioxide endoplasmic reticulum protein folding unfolded protein response Physiology QP1-981
spellingShingle	hypercapnia carbon dioxide endoplasmic reticulum protein folding unfolded protein response Physiology QP1-981 Vitalii Kryvenko Vitalii Kryvenko István Vadász István Vadász István Vadász Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
description	Protein transcription, translation, and folding occur continuously in every living cell and are essential for physiological functions. About one-third of all proteins of the cellular proteome interacts with the endoplasmic reticulum (ER). The ER is a large, dynamic cellular organelle that orchestrates synthesis, folding, and structural maturation of proteins, regulation of lipid metabolism and additionally functions as a calcium store. Recent evidence suggests that both acute and chronic hypercapnia (elevated levels of CO2) impair ER function by different mechanisms, leading to adaptive and maladaptive regulation of protein folding and maturation. In order to cope with ER stress, cells activate unfolded protein response (UPR) pathways. Initially, during the adaptive phase of ER stress, the UPR mainly functions to restore ER protein-folding homeostasis by decreasing protein synthesis and translation and by activation of ER-associated degradation (ERAD) and autophagy. However, if the initial UPR attempts for alleviating ER stress fail, a maladaptive response is triggered. In this review, we discuss the distinct mechanisms by which elevated CO2 levels affect these molecular pathways in the setting of acute and chronic pulmonary diseases associated with hypercapnia.
format	article
author	Vitalii Kryvenko Vitalii Kryvenko István Vadász István Vadász István Vadász
author_facet	Vitalii Kryvenko Vitalii Kryvenko István Vadász István Vadász István Vadász
author_sort	Vitalii Kryvenko
title	Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
title_short	Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
title_full	Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
title_fullStr	Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
title_full_unstemmed	Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction
title_sort	mechanisms of hypercapnia-induced endoplasmic reticulum dysfunction
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/30e9f3fa8d0e470690a5bcd0835f3293
work_keys_str_mv	AT vitaliikryvenko mechanismsofhypercapniainducedendoplasmicreticulumdysfunction AT vitaliikryvenko mechanismsofhypercapniainducedendoplasmicreticulumdysfunction AT istvanvadasz mechanismsofhypercapniainducedendoplasmicreticulumdysfunction AT istvanvadasz mechanismsofhypercapniainducedendoplasmicreticulumdysfunction AT istvanvadasz mechanismsofhypercapniainducedendoplasmicreticulumdysfunction
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Mechanisms of Hypercapnia-Induced Endoplasmic Reticulum Dysfunction

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