From endoplasmic-reticulum stress to the inflammatory response
Kezhong Zhang,Randal J. Kaufman +1 more
TL;DR: New observations suggest that the unfolded-protein response can initiate inflammation, and the coupling of these responses in specialized cells and tissues is now thought to be fundamental in the pathogenesis of inflammatory diseases.
read more
Abstract: The endoplasmic reticulum is responsible for much of a cell's protein synthesis and folding, but it also has an important role in sensing cellular stress. Recently, it has been shown that the endoplasmic reticulum mediates a specific set of intracellular signalling pathways in response to the accumulation of unfolded or misfolded proteins, and these pathways are collectively known as the unfolded-protein response. New observations suggest that the unfolded-protein response can initiate inflammation, and the coupling of these responses in specialized cells and tissues is now thought to be fundamental in the pathogenesis of inflammatory diseases. The knowledge gained from this emerging field will aid in the development of therapies for modulating cellular stress and inflammation.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Oxidative Stress in the Healthy and Wounded Hepatocyte: A Cellular Organelles Perspective
TL;DR: This review recapitulates the evolving concept of oxidative stress in the diverse cellular compartments, highlighting the principle mechanisms of oxidative Stress occurring in the healthy and wounded hepatocyte.
Hydrogen sulfide alleviates hyperhomocysteinemia-mediated skeletal muscle atrophy via mitigation of oxidative and endoplasmic reticulum stress injury.
Avisek Majumder,Mahavir Singh,Jyotirmaya Behera,Nicholas T. Theilen,Akash K. George,Neetu Tyagi,Naira Metreveli,Suresh C. Tyagi +7 more
TL;DR: Evidence is provided that NaHS is beneficial in mitigating HHcy-mediated skeletal injury incited by oxidative/ER stress responses, and functional studies revealed that Na HS administration improved muscle fatigability in CBS+/- mice.
Endoplasmic reticulum stress response and bone loss in experimental periodontitis in mice.
TL;DR: ER stress induced by oral administration of P. gingivalis is involved in alveolar bone resorption independent of inflammatory cytokines in mice, and no effect of 4-PBA was observed for proinflammatory cytokine expression inGingival tissues.
58
Interplay between Inflammation and Cellular Stress Triggered by Flaviviridae Viruses
TL;DR: The new findings that connect the inflammatory pathways to cellular stress sensors and the strategies of Flaviviridae members to counteract these cellular mechanisms and escape immune response are reviewed.
BAG2 ameliorates endoplasmic reticulum stress-induced cell apoptosis in Mycobacterium tuberculosis-infected macrophages through selective autophagy
TL;DR: It is indicated that BAG2 has anti-apoptotic effects on M. tuberculosis-induced ER stress, which is dependent on the promotion of autophagic flux and the induction of selective autophagy.
58
References
Inflammation and metabolic disorders
TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
Signal integration in the endoplasmic reticulum unfolded protein response
David Ron,Peter Walter +1 more
TL;DR: Together, at least three mechanistically distinct arms of the UPR regulate the expression of numerous genes that function within the secretory pathway but also affect broad aspects of cell fate and the metabolism of proteins, amino acids and lipids.
6.3K
Calcium signalling: dynamics, homeostasis and remodelling
TL;DR: The Ca2+-signalling toolkit is used to assemble signalling systems with very different spatial and temporal dynamics and has a direct role in controlling the expression patterns of its signalling systems that are constantly being remodelled in both health and disease.
Signal transduction by the JNK group of MAP kinases.
TL;DR: This review will focus on the JNK group of MAP kinases, which are characterized by the sequence TEY and the two stress-activatedMAP kinases: p38 with the sequence TGY, and the c-Jun NH2-terminal kinases (JNK) with the sequences TPY.
4.4K
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Umut Ozcan,Qiong Cao,Erkan Yilmaz,Ann-Hwee Lee,Neal N. Iwakoshi,Esra Özdelen,Gurol Tuncman,Cem Z. Görgün,Laurie H. Glimcher,Gökhan S. Hotamisligil +9 more
TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).
3.8K