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Advances in Endoplasmic Reticulum Stress and Apoptosis—Second Edition
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Advances in Endoplasmic Reticulum Stress and Apoptosis—Second Edition

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

Deadline for manuscript submissions: 20 May 2026 | Viewed by 1474

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
Special Issues, Collections and Topics in MDPI journals
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 Issues, Collections and Topics in MDPI journals

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 the ER lumen leads to ER stress, which primarily triggers the adaptive functions of the UPR to avoid cell damage. If readjustment efforts fail, then unresolved ER stress can lead to cell death mechanisms including apoptosis and other newly described cell-killing processes. It has also been posited that autophagy is initiated by ER stress as a protective pathway against cell damage. The role of ER stress is becoming increasingly important in a wide range of human diseases; it is crucial that we continue to investigate its effects as thoroughly as possible.

The aim of this Special Issue is to showcase current developments, challenges, and benefits in studying ER stress and related signalling pathways. This Special Issue will include both review articles and original research papers that address the diversity of pathways in cell death initiated by ER imbalance and their involvement 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 250 words) can be sent to the Editorial Office for assessment.

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

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Published Papers (2 papers)

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Research

19 pages, 2036 KB  
Article
Resveratrol-Supported Bioenergetics Leads to Higher Productivity and Accompanying Endoplasmic Reticulum Stress in a mAb-Producing CHO Cell Line
by Bálint Kurucz, Péter Hajdinák and András Szarka
Int. J. Mol. Sci. 2025, 26(22), 11146; https://doi.org/10.3390/ijms262211146 - 18 Nov 2025
Viewed by 654
Abstract
Increasingly unpredictable market demands and the growing market of biosimilars all facilitate lower manufacturing costs. Cell culture media additives have significant potential to improve cell-specific productivity. It has been reported that the treatment of CHO cells with resveratrol results in a reduction in [...] Read more.
Increasingly unpredictable market demands and the growing market of biosimilars all facilitate lower manufacturing costs. Cell culture media additives have significant potential to improve cell-specific productivity. It has been reported that the treatment of CHO cells with resveratrol results in a reduction in viable cell density and a significant increase in cell-specific productivity. In the present study, we apply our knowledge of resveratrol gained on immortal cell lines to elucidate the details of resveratrol’s effects on mAb-producing CHO cells. In the present study, we confirm that resveratrol causes cell cycle arrest, which results in the increased protein productivity of mAb-producing cells. We demonstrate for the first time that resveratrol induces ER stress in mAb-producing CHO lines, presumably by increasing the amount of specific protein produced. It was found that ER stress did not induce oxidative stress, and cell viability could not be enhanced by apoptosis, necroptosis, or ferroptosis inhibitors. Therefore, these cell deaths may not play a role in the process. We also describe, for the first time, that resveratrol is able to increase ATP levels in mAb-producing CHO cells, thereby providing additional energy to mAb-producing CHO cells. This increased ATP synthesis is likely due to the intensification of respiration, not an increase in the number of mitochondria. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis—Second Edition)
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19 pages, 500 KB  
Article
Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival—A Mathematical Study
by Marianna Holczer, Margita Márton, Ibolya Stiller, Beáta Lizák, Gábor Bánhegyi and Orsolya Kapuy
Int. J. Mol. Sci. 2025, 26(22), 10961; https://doi.org/10.3390/ijms262210961 - 12 Nov 2025
Viewed by 479
Abstract
Proper functioning of the endoplasmic reticulum (ER) plays a key role in maintaining the internal homeostasis of the cell. A common feature of many common diseases (such as diabetes and inflammatory bowel diseases) is the induction of ER stress in cells. While some [...] Read more.
Proper functioning of the endoplasmic reticulum (ER) plays a key role in maintaining the internal homeostasis of the cell. A common feature of many common diseases (such as diabetes and inflammatory bowel diseases) is the induction of ER stress in cells. While some ER stress is beneficial for cellular survival, high levels of stress can lead to cell death. For this reason, many studies are focused on understanding the exact mechanism of the ER stress response. There are a variety of well-established stressors on the market that can be used to induce ER stress under laboratory conditions (i.e., thapsigargin and tunicamycin). However, new scientific results suggest that these ER stressors act very differently on the stress response mechanism and, therefore, cannot always be used reliably. By using various mathematical methods, our systems biology approach presented here seeks to answer how the well-known ER stressors affect the dynamic characteristic of the control network, specifically highlighting how we can delay the negative impact of ER stress. Furthermore, using mathematical models, we make suggestions on which ER stressors may be useful in which therapeutic treatment. Full article
(This article belongs to the Special Issue Advances in Endoplasmic Reticulum Stress and Apoptosis—Second Edition)
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