ER remodeling via ER-phagy

Gubaš, Andrea; Đikić, Ivan

doi:10.1016/j.molcel.2022.02.018

Cited by 46 publications

(43 citation statements)

References 89 publications

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“…ROS induced liver cell apoptosis is closely related to endoplasmic reticulum stress signaling pathway. The endoplasmic reticulum is an essential site for protein synthesis in the organism, which is critical for the immune defence function of the organism (34)(35)(36)(37)(38). GRP78 is a key transmembrane protein in the endoplasmic reticulum and plays a key role in the adjustion of endoplasmic reticulum function.…”

Section: Discussionmentioning

confidence: 99%

Zinc Deficiency Induces Endoplasmic Reticulum Stress Leading To Hepatocyte Apoptosis in Mice

Cui

Wang

Deng

et al. 2022

Preprint

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Zinc (Zn) is a crucial trace element for the organism. We investigated Zn deficiency causing endoplasmic reticulum stress and apoptosis by establishing a mouse Zn deficiency model (34 mg/kg in CG group and 2 mg/kg in LG group) and hepatocyte Zn deficiency model (add 0 umol TPEN in CCG group, add 50 umol TPEN in C50 group, add 100 umol TPEN in C100 group). The Zn deficiency caused oxidative stress and produced a large amount of ROS, which had a greater effect on the endoplasmic reticulum and caused endoplasmic reticulum stress. HE staining, liver tissue showed more inflammatory cell infiltration, and TUNEL showed that more apoptotic cells appeared in the LG group compared with the CG group. In RT-PCR assay, we found that the expression of GRP78, IRE-1α, ATF6, PERK, and Chop gene increased in the Zn deficiency group, and caspase-12, caspase-9, caspase-3, caspase-7, PARP apoptotic gene expression were increased. In the apoptosis assay, AO/EB staining clearly showed an increase in apoptotic cells in the Zn-deficient group. Our study provides some basis for the effects of trace element Zn on the liver in terms of endoplasmic reticulum stress.

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Section: Discussionmentioning

confidence: 99%

Zinc Deficiency Induces Endoplasmic Reticulum Stress Leading To Hepatocyte Apoptosis in Mice

Cui

Wang

Deng

et al. 2022

Preprint

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“…Morphologically, it resembles a net-like array structure composed of connected sacs and branching tubules (Figure 3A). The ER has multiple functions, including the synthesis of lipids and proteins, Ca 2+ storage, the folding and transport of membrane and secretory proteins, and communication with other organelles [66]. In addition to these known functions, the ER also plays a role in regulating the assembly and disassembly of non-membrane granules such as processing bodies (P-bodies) and stress granules [67].…”

Section: Lipid-mediated Phase Separation Of Agos On the Er And Their ...mentioning

confidence: 99%

Argonaute-dependent ribosome-associated protein quality control

Gao

Zhu

Sun

et al. 2023

Trends in Cell Biology

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“…Given its complexity, the ER is a highly dynamic organelle that undergoes continuous remodeling to accommodate the changing demands in cellular protein homeostasis. The selective autophagic degradation of the ER, known as ER-phagy, substantially contributes to the ER remodeling process ( Wilkinson, 2019 ; Gubas and Dikic, 2022 ).…”

Section: Er-phagymentioning

confidence: 99%

Metabolic adaption of cancer cells toward autophagy: Is there a role for ER-phagy?

Gentile

Esposito

2022

Front. Mol. Biosci.

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Autophagy is an evolutionary conserved catabolic pathway that uses a unique double-membrane vesicle, called autophagosome, to sequester cytosolic components, deliver them to lysosomes and recycle amino-acids. Essentially, autophagy acts as a cellular cleaning system that maintains metabolic balance under basal conditions and helps to ensure nutrient viability under stress conditions. It is also an important quality control mechanism that removes misfolded or aggregated proteins and mediates the turnover of damaged and obsolete organelles. In this regard, the idea that autophagy is a non-selective bulk process is outdated. It is now widely accepted that forms of selective autophagy are responsible for metabolic rewiring in response to cellular demand. Given its importance, autophagy plays an essential role during tumorigenesis as it sustains malignant cellular growth by acting as a coping-mechanisms for intracellular and environmental stress that occurs during malignant transformation. Cancer development is accompanied by the formation of a peculiar tumor microenvironment that is mainly characterized by hypoxia (oxygen < 2%) and low nutrient availability. Such conditions challenge cancer cells that must adapt their metabolism to survive. Here we review the regulation of autophagy and selective autophagy by hypoxia and the crosstalk with other stress response mechanisms, such as UPR. Finally, we discuss the emerging role of ER-phagy in sustaining cellular remodeling and quality control during stress conditions that drive tumorigenesis.

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ER remodeling via ER-phagy

Cited by 46 publications

References 89 publications

Zinc Deficiency Induces Endoplasmic Reticulum Stress Leading To Hepatocyte Apoptosis in Mice

Zinc Deficiency Induces Endoplasmic Reticulum Stress Leading To Hepatocyte Apoptosis in Mice

Argonaute-dependent ribosome-associated protein quality control

Metabolic adaption of cancer cells toward autophagy: Is there a role for ER-phagy?

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