The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
Stress, Inflammation, and Defense of Homeostasis
Open accessAbstract
Inflammation is traditionally considered a defense response induced by infection or injury. However, inflammation can also be induced by tissue stress and malfunction in the absence of infection or overt tissue damage. Here we discuss the relationship between homeostasis, stress responses, and inflammation. Stress responses have cell-autonomous and cell-extrinsic components, the latter contributing to tissue level adaptation to stress conditions. Inflammation can be thought of as the extreme end of a spectrum that ranges from homeostasis to stress response to bona fide inflammatory response. Inflammation can be triggered by two types of stimuli: extreme deviations of homeostasis or challenges that cause a disruption of homeostasis. This perspective may help to explain qualitative differences and functional outcomes of diverse inflammatory responses.
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“Inflammation is theorized to be a unifying feature of homeostatic perturbation: providing a protective response to extreme deviations from the homeostatic set point174,175.”
From Neural mechanisms of social homeostasis (2019) · cites this paper as [174]
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“In contrast, several studies found that sleep reduces neutrophil counts (69, 112, 178, 287, 326, 338, 480, 580), although again some studies did not find any changes (67, 103, 122, 469).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [112]
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Cites
Inflammation and metabolic disorders
Hotamisligil, G. S. (2006) · Nature · doi:10.1038/nature05485 · Cited by 9,199
Exploring the full spectrum of macrophage activation
Mosser, D. M., & Edwards, J. P. (2008) · Nature Reviews Immunology · doi:10.1038/nri2448 · Cited by 9,144
Pattern Recognition Receptors and Inflammation
Takeuchi, O., & Akira, S. (2010) · Cell · doi:10.1016/j.cell.2010.01.022 · Cited by 8,895
Origin and physiological roles of inflammation
Medzhitov, R. (2008) · Nature · doi:10.1038/nature07201 · Cited by 6,618
Self-citationVascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis
Shweiki, D., Itin, A., Soffer, D., & Keshet, E. (1992) · Nature · doi:10.1038/359843a0 · Cited by 4,617
Cellular and Molecular Mechanisms of Pain
Basbaum, A. I., Bautista, D. M., Scherrer, G., & Julius, D. (2009) · Cell · doi:10.1016/j.cell.2009.09.028 · Cited by 4,344
Inflammatory Mechanisms in Obesity
Gregor, M. F., & Hotamisligil, G. S. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-031210-101322 · Cited by 3,754
Autophagy and the Integrated Stress Response
Kroemer, G., Mariño, G., & Levine, B. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.023 · Cited by 3,506
CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis
Qian, B.-Z., Li, J., Zhang, H., Kitamura, T., Zhang, J., Campion, L. R., Kaiser, E. A., Snyder, L. A., & Pollard, J. W. (2011) · Nature · doi:10.1038/nature10138 · Cited by 2,874
Endoplasmic reticulum stress and the inflammatory basis of metabolic disease
Hotamisligil, G. S. (2010) · Cell · doi:10.1016/j.cell.2010.02.034 · Cited by 2,802
Cited by
Sorted by citations
Control of adaptive immunity by the innate immune system
Iwasaki, A., & Medzhitov, R. (2015) · Nature Immunology · doi:10.1038/ni.3123 · Cited by 2,160
Self-citationThe Sleep-Immune Crosstalk in Health and Disease
Besedovsky, L., Lange, T., & Haack, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00010.2018 · Cited by 1,479
“The typical inflammatory response is triggered by a local infection or tissue injury, involving PAMPs and DAMPs, and is traditionally thought of as a protective reaction that defends and restores physiological functions (111, 296).”
BackgroundRole of tumor microenvironment in tumorigenesis
Wang, M., Zhao, J., Zhang, L., Wei, F., Lian, Y., Wu, Y., Gong, Z., Zhang, S., Zhou, J., Cao, K., et al. (2017) · Journal of Cancer · doi:10.7150/jca.17648 · Cited by 1,404
Homeostasis, Inflammation, and Disease Susceptibility
Kotas, M. E., & Medzhitov, R. (2015) · Cell · doi:10.1016/j.cell.2015.02.010 · Cited by 1,213
Self-citationSarin, S. K., Choudhury, A. K., Sharma, M. K., Maiwall, R., Mahtab, M. A., Rahman, S., Saigal, S., Saraf, N., Soin, A. S., Devarbhavi, H. C., et al. (2019) · Hepatology International · doi:10.1007/s12072-019-09946-3 · Cited by 904
Metadata
- Authors
- Chovatiya, R., & Medzhitov, R.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Medzhitov, Ruslan
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 54
- Issue
- 2
- Pages
- 281-288
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC4048989
- OpenAlex
- W1975024842
- Cited by
- 704
- References
- 54
- Citations by year
- 2026: 42 · 2025: 66 · 2024: 60 · 2023: 57 · 2022: 80 · 2021: 72 · 2020: 63 · 2019: 64 · 2018: 54 · 2017: 54 · 2016: 51 · 2015: 31 · 2014: 8
- FWCI
- 4.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Blavatnik Family Foundation
- National Institutes of Health (AI046688)
- National Institute of General Medical Sciences (T32GM007205)
- National Institute of Allergy and Infectious Diseases (R37AI046688, AI046688)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- inflammation, homeostasis, tissue stress, stress response, tissue adaptation
- MeSH terms
- Gene Expression Regulation, HeLa Cells, Homeostasis, Humans, Inflammation, Models, Biological, Stress, Physiological
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