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Cited by 358

The DOI matches its Crossref record; 91 of the 91 references it cites were found in a registry or an index.

The innate immune response in ischemic acute kidney injury

Open access
Jang, Hye Ryoun, Rabb, Hamid·2009·Clinical Immunology

Abstract

Kidney ischemia reperfusion injury is a major cause of morbidity in both allograft and native kidneys. Ischemia reperfusion-induced acute kidney injury is characterized by early, allo-antigen independent inflammation. Major components of the innate immune system are activated and participate in the pathogenesis of acute kidney injury, plus prime the allograft kidney for rejection. Soluble members of innate immunity implicated in acute kidney injury include the complement system, cytokines, and chemokines. Toll-like receptors (TLRs) are also important contributors. Effector cells that participate in ACUTE KIDNEY INJURY include the classic innate immune cells, neutrophils and macrophages. Recent data has unexpectedly identified lymphocytes as participants of early acute kidney injury responses. In this review, we will focus on immune mediators that participate in the pathogenesis of ischemic acute kidney injury.

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Crossref · 10.1016/j.clim.2008.08.016

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Metadata

Authors
Jang, H. R., & Rabb, H.
Venue
Clinical Immunology
Publisher
Elsevier BV
Published
2009-01
Volume
130
Issue
1
Pages
41-50
ISSN
1521-6616 (ISSN-L)
OpenAlex
W1964536962
Cited by
358
References
91
FWCI
14.88
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: The innate immune response in ischemic acute kidney injury. https://app.cochat.ai/papers/10.1016/j.clim.2008.08.016
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Jang, H. R., & Rabb, H. (2009). The innate immune response in ischemic acute kidney injury. Clinical Immunology. https://doi.org/10.1016/j.clim.2008.08.016

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.