Endoplasmic Reticulum Stress and Human Disease: Lessons from Animal Models

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 June 2025) | Viewed by 2263

Editor


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Guest Editor
Laboratoire de Génétique et Biologie Cellulaire, UR4589, Université de Versailles Saint-Quentin-en-Yvelines/Université Paris-Saclay, Batiment Simone Veil 2 Avenue de la Source de la Bièvre, 78180 Montigny-le-Bretonneux, France
Interests: ER stress; cell death; drosophila; UPR; stress response

Special Issue Information

Dear Colleagues,

The endoplasmic reticulum (ER) is a central hub for protein synthesis and processing. It is key to lipid synthesis and indispensable for maintaining calcium homeostasis. Disruptions in ER function can precipitate ER stress, a cellular response that has been linked to a diverse spectrum of human diseases, encompassing neurodegenerative disorders, diabetes, cardiovascular conditions, and various cancers. Interestingly, ER stress has also been associated with physiological processes.

This Special Issue of Cells is dedicated to uncovering the complex interplay between ER stress and disease pathology. A focal point of this Issue is related research on animal models, which offer a controlled experimental framework to elucidate the physiological impacts of ER stress. These models are crucial for dissecting the pathomechanisms of diseases driven by ER stress, providing a deeper understanding of the molecular and cellular dynamics at play.

This Issue will delve into the cellular and molecular intricacies of ER stress, its contribution to the etiology of certain diseases, and the prospects for developing targeted therapeutic strategies. We encourage submissions of both original research and comprehensive reviews that contribute to our collective understanding of ER stress and its implications for human health.

We warmly invite researchers to submit their work to this Special Issue, and we eagerly anticipate collaborating with the scientific community to disseminate these vital findings through their publication in Cells.

Dr. Sébastien Gaumer
Guest Editor

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Keywords

  • endoplasmic reticulum (ER)
  • ER stress
  • human diseases
  • neurodegenerative disorders
  • diabetes
  • cardiovascular diseases
  • cancer
  • animal models
  • pathomechanisms
  • therapeutic strategies

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Published Papers (1 paper)

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Review

24 pages, 6127 KB  
Review
Deciphering Roles of Placental Endoplasmic Reticulum Stress in Complicated Pregnancies and Beyond: The Power of Mouse Models
by Hong Wa Yung, Yat Nam Yung, Graham J. Burton and D. Stephen Charnock-Jones
Cells 2026, 15(2), 96; https://doi.org/10.3390/cells15020096 - 6 Jan 2026
Viewed by 1741
Abstract
Over a quarter of human pregnancies are associated with complications, including fetal growth restriction, pre-eclampsia and gestational diabetes. These are major causes of maternal and fetal morbidity and mortality, and also lead to a 3–5-fold increased risk of subsequent development of cardio-metabolic diseases. [...] Read more.
Over a quarter of human pregnancies are associated with complications, including fetal growth restriction, pre-eclampsia and gestational diabetes. These are major causes of maternal and fetal morbidity and mortality, and also lead to a 3–5-fold increased risk of subsequent development of cardio-metabolic diseases. Although the mechanistic details remain elusive, a dysfunctional placenta is central to the pathophysiology of these conditions. The placenta ensures sufficient nutrient supply to the fetus without compromising maternal wellbeing. This balance is achieved by the secretion of large quantities of placental-derived peptide hormones into the maternal circulation. Consequently, the placenta is susceptible to endoplasmic reticulum (ER) stress, and we were the first to demonstrate the presence of ER stress in placentas from complicated pregnancies. The mouse placenta provides an ideal model for studying the impact of ER stress as it is composed of two distinct regions, an endocrine zone and a transport zone. Therefore, perturbation of placental endocrine function by ER stress can be generated without directly affecting its capacity for nutrient exchange. In this review, we summarise the current literature on how transgenic mouse models enhance our understanding of ER stress-mediated perturbation of placental endocrine function, and its contribution to the pathophysiology of pregnancy complications and life-long health. Full article
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