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- Title
IKK1 aggravates ischemia–reperfusion kidney injury by promoting the differentiation of effector T cells.
- Authors
Song, Ning; Xu, Yang; Paust, Hans-Joachim; Panzer, Ulf; de las Noriega, Maria Mercedes; Guo, Linlin; Renné, Thomas; Huang, Jiabin; Meng, Xianglin; Zhao, Mingyan; Thaiss, Friedrich
- Abstract
Ischemia–reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI), and experimental work has revealed detailed insight into the inflammatory response in the kidney. T cells and NFκB pathway play an important role in IRI. Therefore, we examined the regulatory role and mechanisms of IkappaB kinase 1 (IKK1) in CD4+T lymphocytes in an experimental model of IRI. IRI was induced in CD4cre and CD4IKK1Δ mice. Compared to control mice, conditional deficiency of IKK1 in CD4+T lymphocyte significantly decreased serum creatinine, blood urea nitrogen (BUN) level, and renal tubular injury score. Mechanistically, lack in IKK1 in CD4+T lymphocytes reduced the ability of CD4 lymphocytes to differentiate into Th1/Th17 cells. Similar to IKK1 gene ablation, pharmacological inhibition of IKK also protected mice from IRI. Together, lymphocyte IKK1 plays a pivotal role in IRI by promoting T cells differentiation into Th1/Th17 and targeting lymphocyte IKK1 may be a novel therapeutic strategy for IRI.
- Publication
Cellular & Molecular Life Sciences, 2023, Vol 80, Issue 5, p1
- ISSN
1420-682X
- Publication type
Article
- DOI
10.1007/s00018-023-04763-2