ER Stress and Redox Regulation in Chronic Inflammation and Disease

Endoplasmic reticulum (ER) stress is increasingly recognized as a central driver of chronic inflammation and immune dysregulation. The unfolded protein response (UPR), a key adaptive mechanism to ER stress, influences immune cell survival, differentiation, and cytokine production, while sustained or unresolved ER stress can promote pathogenic inflammatory signaling and tissue injury.
ER stress does not act in isolation — it intersects with redox imbalance, mitochondrial dysfunction, and metabolic reprogramming, creating a feed-forward loop that sustains chronic inflammatory states. These processes play critical roles in autoimmune diseases, chronic infections, cancer-associated inflammation, and metabolic-inflammatory disorders.

This Research Topic aims to bring together mechanistic and translational studies that elucidate:

-The role of ER stress and UPR signaling in immune cell activation, differentiation, and effector function
-Crosstalk between ER stress, oxidative stress, and mitochondrial pathways in inflammatory pathologies
-ER–mitochondria contact sites and their role in immune and inflammatory regulation
-Therapeutic strategies targeting ER stress and redox pathways to resolve chronic inflammation
-Multi-omics and systems biology approaches to profile ER stress–driven immune phenotypes

By focusing on the convergence of ER stress and redox regulation in inflammation, this Research Topic seeks to advance understanding of disease mechanisms and identify molecular targets for intervention.

Please note: Bibliometric studies and bioinformatic studies based on the analysis of public databases without experimental validation are not in scope for this journal section.