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Advances in Endoplasmic Reticulum Stress and Apoptosis
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Advances in Endoplasmic Reticulum Stress and Apoptosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 2911

Special Issue Editors

Dr. Orsolya Kapuy

E-Mail Website
Guest Editor
Department of Molecular Biology, Semmelweis University, 1094 Budapest, Hungary
Interests: endoplasmic reticulum stress; autophagy; cellular survival; systems biology
Dr. Beáta Lizák

E-Mail Website
Guest Editor
Department of Molecular Biology and Pathobiochemistry, Semmelweis University, 1094 Budapest, Hungary
Interests: endoplasmic reticulum stress; redox homeostasis of ER; ER membrane transporters

Special Issue Information

Dear Colleagues,

The endoplasmic reticulum (ER) acts as an essential integrator of external and internal stimuli in order to preserve cellular homeostasis. This process is tightly regulated by a complex network of signalling pathways called the unfolded protein response (UPR). The accumulation of incorrectly folded proteins or metabolic imbalance in ER lumen leads to ER stress, which primarily triggers the adaptive functions of UPR to avoid cell damage. If readjustment efforts fail, unresolved ER stress can lead to cell death mechanisms including apoptosis and other newly described cell killing processes. Autophagy was also claimed to be initiated by ER stress as a protective pathway from cell damage. The role of ER stress is becoming increasingly important in a wide range of human diseases; it is always appropriate to update its effects as thoroughly as possible.

The goal of this Special Issue is to showcase both the development and the current challenges/benefits of studying ER stress and the related signalling pathways. This Special Issue will include both review articles and original research papers to address the diversity of pathways in cell death initiated by ER imbalance and their integration in various diseases.

Dr. Orsolya Kapuy
Dr. Beáta Lizák
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ER stress
  • apoptosis initiated by ER stress
  • cellular survival
  • redox homeostasis of ER
  • autophagy initiated by ER stress
  • cell death pathways initiated by ER stress

Published Papers (4 papers)

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Research

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18 pages, 2728 KiB  
Article
D-Allulose Reduces Hypertrophy and Endoplasmic Reticulum Stress Induced by Palmitic Acid in Murine 3T3-L1 Adipocytes
by Maria Sofia Molonia, Federica Lina Salamone, Antonio Speciale, Antonella Saija and Francesco Cimino
Int. J. Mol. Sci. 2024, 25(7), 4059; https://doi.org/10.3390/ijms25074059 - 05 Apr 2024
Viewed by 506
Abstract
Natural rare sugars are an alternative category of sweeteners with positive physiologic and metabolic effects both in in vitro and animal models. D-allulose is a D-fructose epimer that combines 70% sucrose sweetness with the advantage of an extremely low energy content. However, there [...] Read more.
Natural rare sugars are an alternative category of sweeteners with positive physiologic and metabolic effects both in in vitro and animal models. D-allulose is a D-fructose epimer that combines 70% sucrose sweetness with the advantage of an extremely low energy content. However, there are no data about the effect of D-allulose against adipose dysfunction; thus, it remains to be confirmed whether D-allulose is useful in the prevention and in treatment of adipose tissue alterations. With this aim, we evaluated D-allulose’s preventive effects on lipid accumulation in 3T3-L1 murine adipocytes exposed to palmitic acid (PA), a trigger for hypertrophic adipocytes. D-allulose in place of glucose prevented adipocyte hypertrophy and the activation of adipogenic markers C/EBP-β and PPARγ induced by high PA concentrations. Additionally, D-allulose pretreatment inhibited the NF-κB pathway and endoplasmic reticulum stress caused by PA, through activation of the Nrf2 pathway. Interestingly, these effects were also observed as D-allulose post PA treatment. Although our data need to be confirmed through in vivo models, our findings suggest that incorporating D-allulose as a glucose substitute in the diet might have a protective role in adipocyte function and support a unique mechanism of action in this sugar as a preventive or therapeutic compound against PA lipotoxicity through the modulation of pathways connected to lipid transport and metabolism. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis)
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20 pages, 2290 KiB  
Article
The Dual Role of Sulforaphane-Induced Cellular Stress—A Systems Biological Study
by Marianna Holczer, Boglárka Besze, Annamária Lehel and Orsolya Kapuy
Int. J. Mol. Sci. 2024, 25(2), 1220; https://doi.org/10.3390/ijms25021220 - 19 Jan 2024
Viewed by 574
Abstract
The endoplasmic reticulum (ER) plays a crucial role in cellular homeostasis. When ER stress is generated, an autophagic self-digestive process is activated to promote cell survival; however, cell death is induced in the case of excessive levels of ER stress. The aim of [...] Read more.
The endoplasmic reticulum (ER) plays a crucial role in cellular homeostasis. When ER stress is generated, an autophagic self-digestive process is activated to promote cell survival; however, cell death is induced in the case of excessive levels of ER stress. The aim of the present study was to investigate the effect of a natural compound called sulforaphane (SFN) upon ER stress. Our goal was to investigate how SFN-dependent autophagy activation affects different stages of ER stress induction. We approached our scientific analysis from a systems biological perspective using both theoretical and molecular biological techniques. We found that SFN induced the various cell-death mechanisms in a concentration- and time-dependent manner. The short SFN treatment at low concentrations promoted autophagy, whereas the longer treatment at higher concentrations activated cell death. We proved that SFN activated autophagy in a mTORC1-dependent manner and that the presence of ULK1 was required for its function. A low concentration of SFN pre- or co-treatment combined with short and long ER stress was able to promote cell survival via autophagy induction in each treatment, suggesting the potential medical importance of SFN in ER stress-related diseases. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis)
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17 pages, 5031 KiB  
Article
Homer1 Protects against Retinal Ganglion Cell Pyroptosis by Inhibiting Endoplasmic Reticulum Stress-Associated TXNIP/NLRP3 Inflammasome Activation after Middle Cerebral Artery Occlusion-Induced Retinal Ischemia
by Weihao Lv, Xiuquan Wu, Yanan Dou, Yiwen Yan, Leiying Chen, Zhou Fei and Fei Fei
Int. J. Mol. Sci. 2023, 24(23), 16811; https://doi.org/10.3390/ijms242316811 - 27 Nov 2023
Cited by 2 | Viewed by 848
Abstract
Retinal ischemia, after cerebral ischemia, is an easily overlooked pathophysiological problem in which inflammation is considered to play an important role. Pyroptosis is a kind of cell death pattern accompanied by inflammation. Homer scaffold protein 1 (Homer1) has anti-inflammation properties and protects against [...] Read more.
Retinal ischemia, after cerebral ischemia, is an easily overlooked pathophysiological problem in which inflammation is considered to play an important role. Pyroptosis is a kind of cell death pattern accompanied by inflammation. Homer scaffold protein 1 (Homer1) has anti-inflammation properties and protects against ischemic injury. However, little is known about pyroptosis following middle cerebral artery occlusion (MCAO)-induced retinal ischemia and the regulatory mechanisms involved by Homer1 for the development of pyroptosis. In the present study, retinal ischemic injury was induced in mice by permanent MCAO in vivo, and retinal ganglion cells (RGCs) were subjected to Oxygen and Glucose Deprivation (OGD) to establish an in vitro model. It was shown that TXNIP/NLRP3-mediated pyroptosis was located predominantly in RGCs, which gradually increased after retinal ischemia and peaked at 24 h after retinal ischemia. Interestingly, the RGCs pyroptosis occurred not only in the cell body but also in the axon. Notably, the occurrence of pyroptosis coincided with the change of Homer1 expression in the retina after retinal ischemia and Homer1 also co-localized with RGCs. It was demonstrated that overexpression of Homer1 not only alleviated RGCs pyroptosis and inhibited the release of pro-inflammatory factors but also led to the increase in phosphorylation of AMPK, inhibition of ER stress, and preservation of visual function after retinal ischemia. In conclusion, it was suggested that Homer1 may protect against MCAO-induced retinal ischemia and RGCs pyroptosis by inhibiting endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation after MCAO-induced retinal ischemia. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis)
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Review

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17 pages, 1526 KiB  
Review
Mechanism of Decision Making between Autophagy and Apoptosis Induction upon Endoplasmic Reticulum Stress
by Orsolya Kapuy
Int. J. Mol. Sci. 2024, 25(8), 4368; https://doi.org/10.3390/ijms25084368 - 15 Apr 2024
Viewed by 261
Abstract
Dynamic regulation of the cellular proteome is mainly controlled in the endoplasmic reticulum (ER). Accumulation of misfolded proteins due to ER stress leads to the activation of unfolded protein response (UPR). The primary role of UPR is to reduce the bulk of damages [...] Read more.
Dynamic regulation of the cellular proteome is mainly controlled in the endoplasmic reticulum (ER). Accumulation of misfolded proteins due to ER stress leads to the activation of unfolded protein response (UPR). The primary role of UPR is to reduce the bulk of damages and try to drive back the system to the former or a new homeostatic state by autophagy, while an excessive level of stress results in apoptosis. It has already been proven that the proper order and characteristic features of both surviving and self-killing mechanisms are controlled by negative and positive feedback loops, respectively. The new results suggest that these feedback loops are found not only within but also between branches of the UPR, fine-tuning the response to ER stress. In this review, we summarize the recent knowledge of the dynamical characteristic of endoplasmic reticulum stress response mechanism by using both theoretical and molecular biological techniques. In addition, this review pays special attention to describing the mechanism of action of the dynamical features of the feedback loops controlling cellular life-and-death decision upon ER stress. Since ER stress appears in diseases that are common worldwide, a more detailed understanding of the behaviour of the stress response is of medical importance. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis)
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