Mitochondria at the interface between danger signaling and metabolism: role of unfolded protein responses in chronic inflammation - PubMed (original) (raw)
Review
. 2012 Jul;18(7):1364-77.
doi: 10.1002/ibd.21944. Epub 2011 Dec 19.
Affiliations
- PMID: 22183876
- DOI: 10.1002/ibd.21944
Review
Mitochondria at the interface between danger signaling and metabolism: role of unfolded protein responses in chronic inflammation
Eva Rath et al. Inflamm Bowel Dis. 2012 Jul.
Abstract
Inflammatory bowel diseases (IBDs), like many other chronic diseases, feature multiple cellular stress responses including endoplasmic reticulum (ER) unfolded protein response (UPR). Maintaining protein homeostasis is indispensable for cell survival and, consequently, distinct signaling pathways have evolved to transmit organelle stress. While the ER UPR, aiming to restore ER homeostasis after challenges to ER function, has been extensively studied in the context of chronic diseases, only recently the related mitochondrial UPR (mtUPR), induced by disturbances of mitochondrial proteostasis, has drawn some attention. ER and mitochondria are in close contact and interact physically and functionally. Accumulating data have placed mitochondria at the center of diverse cellular functions and suggest mitochondria as integrators of signaling pathways such as autophagy and inflammation. Consequently, it is likely that mitochondrial stress and ER stress cannot be regarded separately and that mitochondrial stress, as well as ER stress, participates in the pathology of IBD. Protein homeostasis is particularly sensitive toward infections, oxidative stress, and energy deficiency. Thus, environmental disturbances impacting organelle function lead to the concerted activation of distinct UPRs. The metabolic status might therefore serve as an innate mechanism to sense the epithelial environment, including luminal-derived and host-derived factors. This review highlights mtUPR and its interrelation with ER UPR, focuses on recent studies identifying mitochondria as integrators of cellular danger signaling, and, furthermore, illustrates the importance ER UPR and mitochondrial dysfunction in IBD.
Copyright © 2011 Crohn's & Colitis Foundation of America, Inc.
Similar articles
- Unfolded protein responses in the intestinal epithelium: sensors for the microbial and metabolic environment.
Rath E, Haller D. Rath E, et al. J Clin Gastroenterol. 2012 Oct;46 Suppl:S3-5. doi: 10.1097/MCG.0b013e318264e632. J Clin Gastroenterol. 2012. PMID: 22955354 - Inflammation and cellular stress: a mechanistic link between immune-mediated and metabolically driven pathologies.
Rath E, Haller D. Rath E, et al. Eur J Nutr. 2011 Jun;50(4):219-33. doi: 10.1007/s00394-011-0197-0. Epub 2011 May 1. Eur J Nutr. 2011. PMID: 21547407 Review. - Induction of dsRNA-activated protein kinase links mitochondrial unfolded protein response to the pathogenesis of intestinal inflammation.
Rath E, Berger E, Messlik A, Nunes T, Liu B, Kim SC, Hoogenraad N, Sans M, Sartor RB, Haller D. Rath E, et al. Gut. 2012 Sep;61(9):1269-1278. doi: 10.1136/gutjnl-2011-300767. Epub 2011 Oct 13. Gut. 2012. PMID: 21997551 Free PMC article. - Unfolded Protein Response-Dependent Communication and Contact among Endoplasmic Reticulum, Mitochondria, and Plasma Membrane.
Saito A, Imaizumi K. Saito A, et al. Int J Mol Sci. 2018 Oct 18;19(10):3215. doi: 10.3390/ijms19103215. Int J Mol Sci. 2018. PMID: 30340324 Free PMC article. Review. - Endoplasmic reticulum-mitochondria coupling increases during doxycycline-induced mitochondrial stress in HeLa cells.
Lopez-Crisosto C, Díaz-Vegas A, Castro PF, Rothermel BA, Bravo-Sagua R, Lavandero S. Lopez-Crisosto C, et al. Cell Death Dis. 2021 Jun 28;12(7):657. doi: 10.1038/s41419-021-03945-9. Cell Death Dis. 2021. PMID: 34183648 Free PMC article.
Cited by
- The emerging role of oxidative stress in inflammatory bowel disease.
Muro P, Zhang L, Li S, Zhao Z, Jin T, Mao F, Mao Z. Muro P, et al. Front Endocrinol (Lausanne). 2024 Jul 15;15:1390351. doi: 10.3389/fendo.2024.1390351. eCollection 2024. Front Endocrinol (Lausanne). 2024. PMID: 39076514 Free PMC article. Review. - Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.
Mavroudis CD, Lewis A, Greenwood JC, Kelly M, Ko TS, Forti RM, Shin SS, Shofer FS, Ehinger JK, Baker WB, Kilbaugh TJ, Jang DH. Mavroudis CD, et al. J Med Toxicol. 2024 Jan;20(1):39-48. doi: 10.1007/s13181-023-00971-1. Epub 2023 Oct 17. J Med Toxicol. 2024. PMID: 37847352 - Exploring the potential function of trace elements in human health: a therapeutic perspective.
Islam MR, Akash S, Jony MH, Alam MN, Nowrin FT, Rahman MM, Rauf A, Thiruvengadam M. Islam MR, et al. Mol Cell Biochem. 2023 Oct;478(10):2141-2171. doi: 10.1007/s11010-022-04638-3. Epub 2023 Jan 13. Mol Cell Biochem. 2023. PMID: 36637616 Review. - Mitochondria and Inflammatory Bowel Diseases: Toward a Stratified Therapeutic Intervention.
Ho GT, Theiss AL. Ho GT, et al. Annu Rev Physiol. 2022 Feb 10;84:435-459. doi: 10.1146/annurev-physiol-060821-083306. Epub 2021 Oct 6. Annu Rev Physiol. 2022. PMID: 34614372 Free PMC article. Review. - Targeting Mitochondrial Damage as a Therapeutic for Ileal Crohn's Disease.
Alula KM, Jackson DN, Smith AD, Kim DS, Turner K, Odstrcil E, Kaipparettu BA, Dassopoulos T, Venuprasad K, Feagins LA, Theiss AL. Alula KM, et al. Cells. 2021 May 29;10(6):1349. doi: 10.3390/cells10061349. Cells. 2021. PMID: 34072441 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources