Golgi Stress Response- New Insights into the Pathogenesis and Therapeutic Targets of Human Diseases

Authors
Kim, Won KyuChoi, WooseonDeshar, BarshaKang, ShinwonKim, Jiyoon
Issue Date
2023-04
Publisher
한국분자세포생물학회
Citation
Molecules and Cells, v.46, no.4, pp.191 - 199
Abstract
The Golgi apparatus modifies and transports secretory and membrane proteins. In some instances, the production of secretory and membrane proteins exceeds the capacity of the Golgi apparatus, including vesicle trafficking and the post -translational modification of macromolecules. These proteins are not modified or delivered appropriately due to the insufficiency in the Golgi function. These conditions disturb Golgi homeostasis and induce a cellular condition known as Golgi stress, causing cells to activate the 'Golgi stress response,' which is a homeostatic process to increase the capacity of the Golgi based on cellular requirements. Since the Golgi functions are diverse, several response pathways involving TFE3, HSP47, CREB3, proteoglycan, mucin, MAPK/ ETS, and PERK regulate the capacity of each Golgi function separately. Understanding the Golgi stress response is crucial for revealing the mechanisms underlying Golgi dynamics and its effect on human health because many signaling molecules are related to diseases, ranging from viral infections to fatal neurodegenerative diseases. Therefore, it is valuable to summarize and investigate the mechanisms underlying Golgi stress response in disease pathogenesis, as they may contribute to developing novel therapeutic strategies. In this review, we investigate the perturbations and stress signaling of the Golgi, as well as the therapeutic potentials of new strategies for treating Golgi stress-associated diseases.
Keywords
PROTEIN; ER; TRANSPORT; TRANSCRIPTION; APPARATUS; SPHINGOLIPIDS; TRAFFICKING; METABOLISM; SIGNATURE; MEMBRANE; Golgi stress; Golgi stress response; human disease; pathogenesis; therapeutic target
ISSN
1016-8478
URI

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DOI
10.14348/molcells.2023.2152
Appears in Collections:
KIST Article > 2023
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