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Journal Article

Endoplasmic Reticulum Stress in Aquaculture Species

Noah Esmaeili; Christopher J. Martyniuk; Sunil Kadri; Hongyu Ma
Reviews in Aquaculture · Vol. 17, Issue 3 · 2025

Abstract

Fundamental metabolic functions depend upon the endoplasmic reticulum (ER), as this organelle plays a central role in maintaining cellular homeostasis. Different physiological and pathological conditions can result in the accumulation of misfolded/unfolded proteins, which this accumulation causes ER stress. These pathological conditions can lead to disease and are concerning for species used for aquaculture. In this comprehensive article, we review studies in cultured species that demonstrate the presence of ER stress to understand conditions and events that may underlie this toxicological outcome. Literature indicates that ER stress can be induced by exposure to pollution, environmental factors (salinity, ammonia, nitrate, hypoxia, and temperature), nutritional changes (quality and quantity of protein, lipid, carbohydrate, vitamins, and minerals), and pathogens. ER stress in aquatic species has been demonstrated through tissue histology and microscopy, gene expression analysis, and other omics approaches. In terms of cell signaling for ER stress, the most common gene indicators identified in aquaculture species include grp78 , ire1 , perk , chop , erol, atf4 , atf6 , xbp1 , and eif2 . The ER stress should be minimized in order to divert more energy for individual growth and achieve sustainable and profitable aquaculture. Here, we provide an overview of ER stress in aquatic species and suggest future directions for research.

Bibliographic Information

JournalReviews in Aquaculture
PublisherWiley
Publication Date2025-06-01
Publication Year2025
Volume17
Issue3
Document TypeJournal Article
Print ISSN1753-5123
eISSN1753-5131
DOI10.1111/raq.70036
SubjectGeneral Aquaculture, Fisheries & Fish Science

Access Information

NARA Access Coverage2009-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/17535131
Publisher PageOpen Publisher Page
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