Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Feb;231(2):288-94.
doi: 10.1002/jcp.25098.

Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases

Stewart Siyan Cao  1 , Katherine L Luo  1 , Lynn Shi  1
Affiliations
Review

Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases

Stewart Siyan Cao et al. J Cell Physiol. 2016 Feb.

Abstract

The endoplasmic reticulum (ER) is a critical organelle for normal cell function and homeostasis. Disturbance in the protein folding process in the ER, termed ER stress, leads to the activation of unfolded protein response (UPR) that encompasses a complex network of intracellular signaling pathways. The UPR can either restore ER homeostasis or activate pro-apoptotic pathways depending on the type of insults, intensity and duration of the stress, and cell types. ER stress and the UPR have recently been linked to inflammation in a variety of human pathologies including autoimmune, infectious, neurodegenerative, and metabolic disorders. In the cell, ER stress and inflammatory signaling share extensive regulators and effectors in a broad spectrum of biological processes. In spite of different etiologies, the two signaling pathways have been shown to form a vicious cycle in exacerbating cellular dysfunction and causing apoptosis in many cells and tissues. However, the interaction between ER stress and inflammation in many of these diseases remains poorly understood. Further understanding of the biochemistry, cell biology, and physiology may enable the development of novel therapies that spontaneously target these pathogenic pathways.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abderrazak A, Syrovets T, Couchie D, El Hadri K, Friguet B, Simmet T, Rouis M. 2015. NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases. Redox Biol 4:296–307. - PMC - PubMed
    1. Arisato T, Okubo R, Arata H, Abe K, Fukada K, Sakoda S, Shimizu A, Qin XH, Izumo S, Osame M, Nakagawa M. 2003. Clinical and pathological studies of familial amyotrophic lateral sclerosis (FALS) with SOD1 H46R mutation in large Japanese families. Acta Neuropathol 106:561–568. - PubMed
    1. Atkin JD, Farg MA, Walker AK, McLean C, Tomas D, Horne MK. 2008. Endoplasmic reticulum stress and induction of the unfolded protein response in human sporadic amyotrophic lateral sclerosis. Neurobiol Dis 30:400–407. - PubMed
    1. Benner EJ, Banerjee R, Reynolds AD, Sherman S, Pisarev VM, Tsiperson V, Nemachek C, Ciborowski P, Przedborski S, Mosley RL, Gendelman HE. 2008. Nitrated alpha‐synuclein immunity accelerates degeneration of nigral dopaminergic neurons. PLos ONE 3:e1376. doi: 10.1371/journal.pone.0001376 - DOI - PMC - PubMed
    1. Bodman‐Smith MD, Fife MF, Wythe H, Corrigal VM, Panayi GS, Wedderburn LR, Woo P. 2004. Anti‐BiP antibody levels in juvenile idiopathic arthritis (JIA). Rheumatology 43:1305–1306. - PubMed