The DOI matches its Crossref record; 134 of the 134 references it cites were found in a registry or an index.
Linking oxidative stress to inflammation: Toll-like receptors
Open accessAbstract
Injury caused by oxidative stress occurs in many clinical scenarios involving ischemia and reperfusion such as organ transplantation, hemorrhagic shock (HS), myocardial infarction, and cerebral vascular accidents. Activation of the immune system as a result of disturbances in the redox state of cells seems to contribute to tissue and organ damage in these conditions. The link between oxidative stress and inflammatory pathways is poorly understood. Recently, Toll-like receptors (TLRs) have been shown to mediate the inflammatory response seen in experimental ischemia and reperfusion (I/R). The TLR family of receptors involved in alerting the innate immune system of danger seems to be activated by damage-associated molecular pattern molecules (DAMPs) that are released during conditions of oxidative stress. In this review, we examine the role of TLRs in various experimental models of oxidative stress such as HS and I/R. We also report on potential DAMPs that may interact with TLRs in mediating injury. Finally, potential mechanisms by which reactive oxygen species from NADPH oxidase can signal the commencement of inflammatory pathways through TLRs are explored.
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“Inflammation, in turn, enhances oxidative stress by upregulating the expression of reactive oxygen species–producing enzymes and downregulating antioxidant defenses.126”
From Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association (2011) · cites this paper as [126]
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The Keap1–Nrf2–ARE Pathway As a Potential Preventive and Therapeutic Target: An Update
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The role of oxidative stress during inflammatory processes
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Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus
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Metadata
- Authors
- Gill, R., Tsung, A., & Billiar, T.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Gill, Roop
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 48
- Issue
- 9
- Pages
- 1121-1132
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3423196
- OpenAlex
- W2013742341
- Cited by
- 553
- References
- 134
- Citations by year
- 2026: 21 · 2025: 37 · 2024: 26 · 2023: 41 · 2022: 34 · 2021: 50 · 2020: 42 · 2019: 39 · 2018: 38 · 2017: 33 · 2016: 28 · 2015: 31 · 2014: 35 · 2013: 33 · 2012: 18
- FWCI
- 2.50
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM050441)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- oxidative stress, Toll-like receptors, inflammation, ischemia-reperfusion injury, hemorrhagic shock, damage-associated molecular patterns, reactive oxygen species, NADPH oxidase, innate immunity, organ transplantation, myocardial infarction, stroke
- MeSH terms
- Animals, Humans, Inflammation, Reperfusion Injury, Oxidative Stress, Toll-Like Receptors
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