The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Reactive species mechanisms of cellular hypoxia-reoxygenation injury
Abstract
Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O[Formula: see text]) and release H 2 O 2, a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.
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Cites
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Cited by
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Targeting hypoxic tumor microenvironment in pancreatic cancer
Tao, J., Yang, G., Zhou, W., Qiu, J., Chen, G., Luo, W., Zhao, F., You, L., Zheng, L., Zhang, T., et al. (2021) · Journal of Hematology & Oncology · doi:10.1186/s13045-020-01030-w · Cited by 412
Metadata
- Authors
- Li, C., & Jackson, R. M.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2002-02-01
- Volume
- 282
- Issue
- 2
- Pages
- C227-C241
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2150951327
- Cited by
- 1,043
- References
- 10
- FWCI
- 16.74
- Type
- journal article
- Language
- en
- Open access
- closed
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