Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases
ABSTRACTCells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR),...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2023-12-01
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Series: | Animal Cells and Systems |
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Online Access: | https://www.tandfonline.com/doi/10.1080/19768354.2023.2181217 |
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author | Junhee Kwon Jihyun Kim Keun Il Kim |
author_facet | Junhee Kwon Jihyun Kim Keun Il Kim |
author_sort | Junhee Kwon |
collection | DOAJ |
description | ABSTRACTCells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer. |
first_indexed | 2024-03-08T15:57:10Z |
format | Article |
id | doaj.art-00ea4828892546589abf6feabfe5f3e6 |
institution | Directory Open Access Journal |
issn | 1976-8354 2151-2485 |
language | English |
last_indexed | 2024-03-08T15:57:10Z |
publishDate | 2023-12-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Animal Cells and Systems |
spelling | doaj.art-00ea4828892546589abf6feabfe5f3e62024-01-08T17:12:29ZengTaylor & Francis GroupAnimal Cells and Systems1976-83542151-24852023-12-01271293710.1080/19768354.2023.2181217Crosstalk between endoplasmic reticulum stress response and autophagy in human diseasesJunhee Kwon0Jihyun Kim1Keun Il Kim2Department of Biological Sciences, Sookmyung Women’s University, Seoul, Republic of KoreaDepartment of Biological Sciences, Sookmyung Women’s University, Seoul, Republic of KoreaDepartment of Biological Sciences, Sookmyung Women’s University, Seoul, Republic of KoreaABSTRACTCells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer.https://www.tandfonline.com/doi/10.1080/19768354.2023.2181217Endoplasmic reticulum (ER) stressunfolded protein response (UPR)autophagyhuman diseases |
spellingShingle | Junhee Kwon Jihyun Kim Keun Il Kim Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases Animal Cells and Systems Endoplasmic reticulum (ER) stress unfolded protein response (UPR) autophagy human diseases |
title | Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
title_full | Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
title_fullStr | Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
title_full_unstemmed | Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
title_short | Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
title_sort | crosstalk between endoplasmic reticulum stress response and autophagy in human diseases |
topic | Endoplasmic reticulum (ER) stress unfolded protein response (UPR) autophagy human diseases |
url | https://www.tandfonline.com/doi/10.1080/19768354.2023.2181217 |
work_keys_str_mv | AT junheekwon crosstalkbetweenendoplasmicreticulumstressresponseandautophagyinhumandiseases AT jihyunkim crosstalkbetweenendoplasmicreticulumstressresponseandautophagyinhumandiseases AT keunilkim crosstalkbetweenendoplasmicreticulumstressresponseandautophagyinhumandiseases |