Endoplasmic reticulum stress and therapeutic strategies in metabolic, neurodegenerative diseases and cancer
© 2024. The Author(s)..
The accumulation of unfolded or misfolded proteins within the endoplasmic reticulum (ER), due to genetic determinants and extrinsic environmental factors, leads to endoplasmic reticulum stress (ER stress). As ER stress ensues, the unfolded protein response (UPR), comprising three signaling pathways-inositol-requiring enzyme 1, protein kinase R-like endoplasmic reticulum kinase, and activating transcription factor 6 promptly activates to enhance the ER's protein-folding capacity and restore ER homeostasis. However, prolonged ER stress levels propels the UPR towards cellular demise and the subsequent inflammatory cascade, contributing to the development of human diseases, including cancer, neurodegenerative disorders, and diabetes. Notably, increased expression of all three UPR signaling pathways has been observed in these pathologies, and reduction in signaling molecule expression correlates with decreased proliferation of disease-associated target cells. Consequently, therapeutic strategies targeting ER stress-related interventions have attracted significant research interest. In this review, we elucidate the critical role of ER stress in cancer, metabolic, and neurodegenerative diseases, offering novel therapeutic approaches for these conditions.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:30 |
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| Enthalten in: |
Molecular medicine (Cambridge, Mass.) - 30(2024), 1 vom: 20. März, Seite 40 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yuan, Siqi [VerfasserIn] |
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| Links: |
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| Themen: |
Cancer |
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| Anmerkungen: |
Date Completed 22.03.2024 Date Revised 23.03.2024 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1186/s10020-024-00808-9 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM369991109 |
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| 520 | |a © 2024. The Author(s). | ||
| 520 | |a The accumulation of unfolded or misfolded proteins within the endoplasmic reticulum (ER), due to genetic determinants and extrinsic environmental factors, leads to endoplasmic reticulum stress (ER stress). As ER stress ensues, the unfolded protein response (UPR), comprising three signaling pathways-inositol-requiring enzyme 1, protein kinase R-like endoplasmic reticulum kinase, and activating transcription factor 6 promptly activates to enhance the ER's protein-folding capacity and restore ER homeostasis. However, prolonged ER stress levels propels the UPR towards cellular demise and the subsequent inflammatory cascade, contributing to the development of human diseases, including cancer, neurodegenerative disorders, and diabetes. Notably, increased expression of all three UPR signaling pathways has been observed in these pathologies, and reduction in signaling molecule expression correlates with decreased proliferation of disease-associated target cells. Consequently, therapeutic strategies targeting ER stress-related interventions have attracted significant research interest. In this review, we elucidate the critical role of ER stress in cancer, metabolic, and neurodegenerative diseases, offering novel therapeutic approaches for these conditions | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Cancer | |
| 650 | 4 | |a Endoplasmic reticulum stress | |
| 650 | 4 | |a Metabolic | |
| 650 | 4 | |a Neurodegenerative diseases | |
| 650 | 4 | |a Signaling pathway | |
| 650 | 4 | |a Therapeutic strategies | |
| 700 | 1 | |a She, Dan |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Shangming |e verfasserin |4 aut | |
| 700 | 1 | |a Deng, Nan |e verfasserin |4 aut | |
| 700 | 1 | |a Peng, Jiayi |e verfasserin |4 aut | |
| 700 | 1 | |a Ma, Ling |e verfasserin |4 aut | |
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